PReD-Bench/PRed-Bench huggingface dataset:
Chebulagic acid, a hydrolyzable tannin, exhibited antiviral activity in vitro and in vivo against human enterovirus 71
Authors: Lianfeng Zhang
Chuan Qin
Li Zhang
Yajun Yang
Jiangning Liu
Jinghui Xiu
Xiaoying Li
Yanfeng Xu
Journal: International Journal of Molecular Sciences (2013)
Discipline: CHEMISTRY
Keywords: Human enterovirus 71; hand, foot and mouth disease; children; vaccines; antiviral drugs
Affiliations: Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health, Institute of Laboratory Animal Science, CAMS & Comparative Medicine Centre, PUMC, Beijing 100021, China. .

Abstract:  Human enterovirus 71 is one of the major causative agents of hand, foot and mouth disease in children under six years of age. Presently, no vaccines or antiviral drugs have been clinically available to employ against EV71. In this study, we demonstrate that treatment with chebulagic acid reduced the viral cytopathic effect on rhabdomyosarcoma cells with an IC50 of 12.5 μg/mL. The utilization of the chebulagic acid treatment on mice challenged with a lethal dose of enterovirus 71 was able to efficiently reduce mortality and relieve clinical symptoms through the inhibition of viral replication. Chebulagic acid may represent a potential therapeutic agent to control infections to enterovirus 71. 

Retracted: No

PubPeer comments:
 Retracted on 25 November 2021: https: link.springer.com article 10.1007 s12517-021-09105-9  The Editor-in-Chief and the Publisher have retracted this article because the content of this article is nonsensical. The peer review process was not carried out in accordance with the Publisher s peer review policy. The authors have not responded to correspondence regarding this retraction. Retraction followed after earlier Editorial Expression of Concern: https: link.springer.com article 10.1007 s12517-021-08470-9  Following the publication of this topical collection of the Arabian Journal of Geosciences, the Publisher became aware of serious research integrity concerns within the collection. The peer review process was not carried out in accordance with the Publisheru2019s peer review policy (see https: www.springer.com gp editorial-policies peer-review-policy-process), and may have been deliberately manipulated. All articles in this topical collection are currently being assessed. The Publisher will take further editorial action where appropriate, once this investigation is complete. The authors were informed of the publication of this Editorial Expression of Concern using email addresses provided at submission. This topic has been covered by Retraction Watch: https: retractionwatch.com 2021 09 28 springer-nature-slaps-more-than-400-papers-with-expressions-of-concern-all-at-once ,
Enhancing specific-antibody production to the ragB vaccine with GITRL that expand Tfh, IFN-γ(+) T cells and attenuates Porphyromonas gingivalis infection in mice
Authors: Tianqing Peng
Dong Zheng
Qiang Sun
Zhaoliang Su
Xiaoju Shi
Huaxi Xu
Pei Shen
Shengjun Wang
Jia Tong
Fanzhi Kong
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: RagB; mGITRL; DNA vaccine; immune response; P. gingivalis
Affiliations: Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, Zhenjiang, PR China.

Abstract:  The outer membrane protein RagB is one of the major virulence factors of the periodontal pathogen Porphyromonas gingivalis (P. gingivalis). In order to induce protective immune response against P. gingivalis infection, an mGITRL gene-linked ragB DNA vaccine (pIRES-ragB-mGITRL ) was constructed. Six-week-old female BALB/c mice were immunized with pIRES-ragB-mGITRL through intramuscular injection and then challenged by subcutaneous injection in the abdomen with P. gingivalis. RagB-specific antibody-forming cells were evaluated by an Enzyme-linked immunosorbent spot, and specific antibody was determined by enzyme-linked immunosorbent assay. In addition, the frequencies of Tfh and IFN-γ(+) T cells in spleen were measured using flow cytometer, and the levels of IL-21 and IFN-γ mRNA or proteins were detected by real time RT-PCR or ELISA. The data showed that the mGITRL-linked ragB DNA vaccine induced higher levels of RagB-specific IgG in serum and RagB-specific antibody-forming cells in spleen. The frequencies of Tfh and IFN-γ(+) T cells were obviously expanded in mice immunized by pIRES-ragB-mGITRL compared with other groups (pIRES or pIRES-ragB ). The levels of Tfh and IFN-γ(+) T cells associated cytokines were also significantly increased in pIRES-ragB-mGITRL group. Therefore, the mice immunized with ragB plus mGITRL showed the stronger resistant to P. gingivalis infection and a significant reduction of the lesion size caused by P. gingivalis infection comparing with other groups. Taken together, our findings demonstrated that intramuscular injection of DNA vaccine ragB together with mGITRL induced protective immune response dramatically by increasing Tfh and IFN-γ(+) T cells and antibody production to P. gingivalis. 

Retracted: No

PubPeer comments:
 Figure 3. Reported to the journal in 2015. * Red boxes: the left (COS-7 cells) and right (muscle cells) b-actin panels appear to be identical. Image made lighter to bring out details. ![file] ,
Transposable element persistence via potential genome-level ecosystem engineering
Authors: Brent Saylor
Karl Cottenie
T Ryan Gregory
Stefan Linquist
Stefan C Kremer
Tyler A Elliott
Journal: BMC genomics (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: C-value paradox; Ecosystem engineering; Genome-level ecology; Junk DNA; Transposon accumulation
Affiliations: School of Computer Science, University of Guelph, Guelph, ON, N1G 2W1, Canada. ., Department of Philosophy, University of Guelph, Guelph, ON, N1G 2W1, Canada., Department of Integrative Biology, University of Guelph, Guelph, ON, N1G 2W1, Canada., Centre for Biodiversity Genomics, University of Guelph, Guelph, ON, N1G 2W1, Canada.

Abstract:  Background: The nuclear genomes of eukaryotes vary enormously in size, with much of this variability attributable to differential accumulation of transposable elements (TEs). To date, the precise evolutionary and ecological conditions influencing TE accumulation remain poorly understood. Most previous attempts to identify these conditions have focused on evolutionary processes occurring at the host organism level, whereas we explore a TE ecology explanation. Results: As an alternative (or additional) hypothesis, we propose that ecological mechanisms occurring within the host cell may contribute to patterns of TE accumulation. To test this idea, we conducted a series of experiments using a simulated asexual TE/host system. Each experiment tracked the accumulation rate for a given type of TE within a particular host genome. TEs in this system had a net deleterious effect on host fitness, which did not change over the course of experiments. As one might expect, in the majority of experiments TEs were either purged from the genome or drove the host population to extinction. However, in an intriguing handful of cases, TEs co-existed with hosts and accumulated to very large numbers. This tended to occur when TEs achieved a stable density relative to non-TE sequences in the genome (as opposed to reaching any particular absolute number). In our model, the only way to maintain a stable density was for TEs to generate new, inactive copies at a rate that balanced with the production of active (replicating) copies. Conclusions: From a TE ecology perspective, we suggest this could be interpreted as a case of ecosystem engineering within the genome, where TEs persist by creating their own "habitat". 

Retracted: No

PubPeer comments:
 ![file] ,
Distinct pathways of ERK1/2 activation by hydroxy-carboxylic acid receptor-1
Authors: Li-hui Wang
Hui-qian Wang
Ru-ping Chen
Guo Li
Jun-ping Liu
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: HCA1; ERK1/2 activation; G protein; adenylate cyclase; free fatty acid
Affiliations: Institute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, Zhejiang, China.

Abstract:  Mechanistic investigations have shown that, upon agonist activation, hydroxy-carboxylic acid receptor-1(HCA1) couples to a Gi protein and inhibits adenylate cyclase activity, leading to inhibition of liberation of free fatty acid. However, the underlying molecular mechanisms for HCA1 signaling remain largely unknown. Using CHO-K1 cells stably expressing HCA1, and L6 cells, which endogenously express rat HCA1 receptors, we found that activation of ERK1/2 by HCA1 was rapid, peaking at 5 min, and was significantly blocked by pertussis toxin. Furthermore, time course experiments with different kinase inhibitors demonstrated that HCA1 induced ERK1/2 activation via the extracellular Ca2+, PKC and IGF-I receptor transactivation-dependent pathways. In addition, we observed that pretreated the cells with M119K, an inhibitor of Gβγ subunit-dependent signaling, effectively attenuated the ERK1/2 activation triggered by HCA1, suggesting a critical role for βγ-subunits in HCA1-activated ERK1/2 phosphorylation. Furthermore, the present results also indicated that the arrestin2/3 were not required for ERK1/2 activation. In conclusion, our findings demonstrate that upon binding to agonist, HCA1 receptors initially activate Gi, leading to dissociation of the Gβγ subunit from activated Gi, and subsequently induce ERK1/2 activation via two distinct pathways: one PKC-dependent pathway and the other IGF-IR transactivation-dependent pathway. Our results provide the first in-depth evidence that defines the molecular mechanism of HCA1-mediated ERK1/2 activation. 

Retracted: No

PubPeer comments:
 Figures 3, 4, and 6. * Red boxes: Three lanes in Figure 3A s ERK blot look similar to three lanes in Figure 3B s ERK blot. Note a slanted scratch. * Green boxes: The same two lanes, but in mirror image appear to be visible in FIgure 4B s DMSOO and Go6983 blots. Note a dot and scratches. * Blue boxes: Six ERK lanes in Figure 3B look similar to six lanes in Figure 6B s ERK blot Reported to the journal in October 2015, but no action taken as of today. ![file] ,
Downregulation of ADAM10 expression inhibits metastasis and invasiveness of human hepatocellular carcinoma HepG2 cells
Authors: Lei Shi
Zuoren Wang
Yuan Shao
Yuan Yue
Qing Luo
Journal: BioMed Research International (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ADAM10 expression; metastasis; invasiveness; HepG2 cells; cell migration
Affiliations: Department of Pharmacy, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China., Department of the Otorhinolaryngology, First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi'an, Shaanxi 710061, China, Department of General Surgery, The 417 Hospital of Nuclear Industry, Xi'an, Shaanxi 710600, China, Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi'an, Shaanxi 710061, China

Abstract:  Objective: This study aims to investigate the effects of ADAM10 expression on metastasis and invasiveness of human hepatocellular carcinoma HepG2 cells. Methods: The HepG2 cells were transfected with medium only, the empty vector, the control siRNA, or siRNA against ADAM10, respectively. Cell migration assay and Transwell invasiveness assay were performed to detect the effects of ADAM10 knockdown on migration and invasiveness of HepG2 cells. Western blotting and real-time RT PCR were performed to investigate the effects of knock-down of ADAM10 on protein and mRNA levels of E-cadherin gene. Results: Cell migration and invasiveness of HepG2 cells transfected with ADAM10 siRNA were significantly decreased, when compared with the cells transfected with the control siRNA, suggesting that the downregulation of ADAM10 expression inhibits cell migration and invasiveness. The Western blotting results suggest that the down-regulation of ADAM10 expression increases E-cadherin protein levels. The real-time RT-PCR results indicated that the mRNA level of E-cadherin is not detectably affected by the knock-down of ADAM10 gene. Conclusions: Expression of ADAM10 may be related to cell migration and invasiveness of human hepatocellular carcinoma HepG2 cells via a mechanism related to E-cadherin. 

Retracted: No

PubPeer comments:
 I feel like this article is dangerous and will pose more problem to trans-sexuals in Malaysia. ,
Bees increase crop yield in an alleged pollinator-independent almond variety
Authors: Pedro Negri
Agustin Sáez
Sandra Medici
Marcelo A Aizen
Matias Viel
Ethel Villalobos
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Wild pollinators; managed honey bee colonies; pollination demand; breeding programs; pollinator-dependent crops
Affiliations: Grupo de Ecología de la Polinización, INIBIOMA, CONICET-Universidad Nacional del Comahue, San Carlos de Bariloche, Rio Negro, Argentina. ., Grupo de Ecología de la Polinización, INIBIOMA, CONICET-Universidad Nacional del Comahue, San Carlos de Bariloche, Rio Negro, Argentina., Centro de Investigación en Abejas Sociales (CIAS) (IIPROSAM-CONICET), Universidad Nacional de Mar del Plata (UNMdP), Funes 3350, CP 7600, Mar del Plata, Argentina., Beeflow Inc. - Smart Pollination Services, Los Angeles, CA, USA., Department of Plant and Environmental Sciences, University of Hawaii at Manoa, Honolulu, HI, 96822, USA.

Abstract:  Wild pollinators are declining and the number of managed honey bee colonies is growing slower than agricultural demands for pollination. Because of these contrasting trends in pollinator demand and availability, breeding programs for many pollinator-dependent crops have focused on reducing the need for pollinators. Although numerous crop varieties are now available in the market with the label of pollinator-independent, the real dependence of these varieties on pollinators is mostly unknown. We evaluated the hypothesis of pollinator independence in the Independence almond variety, the fastest growing variety in California that is the main almond production region in the world. In this presumed pollinator-independent variety, we measured the effect of honey bees on fruit set, yield, and kernel nutritional quality at tree level. Fruit set was 60% higher in bee-pollinated than bee-isolated trees, which translated into a 20% increase in kernel yield. Despite its effect on almond production, there was no evidence that bee visitation affected almond nutritional quality. Based on these results, we recommend the use of bees, whether they are wild or managed, to maximize yield even in self-fertile almond varieties. 

Retracted: No

PubPeer comments:
 An interesting piece of research. One thing I don t understand, however, is why, in the mixed model analyses, the nesting of flowers within branches, and of branches within trees, was not also accounted for. Perhaps there is not enough data to estimate all these terms, but it seems to me that this clustering could have important effects, and that some sort of regularised Bayesian analysis could have dealt with it. ,
RETRACTED ARTICLE: The association between early career informal mentorship in academic collaborations and junior author performance
Authors: Kinga Makovi
Bedoor AlShebli
Talal Rahwan
Journal: Nature Communications (2020)
Discipline: Multidisciplinary
Keywords: mentorship; scientific collaborations; senior collaborators; junior scientist; mentor-protégé pairs
Affiliations: Department of Computer Science, Science Division, New York University Abu Dhabi, Abu Dhabi, UAE. ., Computational Social Science Lab, Social Science Division, New York University Abu Dhabi, Abu Dhabi, UAE. ., Social Research and Public Policy, Social Science Division, New York University Abu Dhabi, Abu Dhabi, UAE.

Abstract:  We study mentorship in scientific collaborations, where a junior scientist is supported by potentially multiple senior collaborators, without them necessarily having formal supervisory roles. We identify 3 million mentor-protégé pairs and survey a random sample, verifying that their relationship involved some form of mentorship. We find that mentorship quality predicts the scientific impact of the papers written by protégés post mentorship without their mentors. We also find that increasing the proportion of female mentors is associated not only with a reduction in post-mentorship impact of female protégés, but also a reduction in the gain of female mentors. While current diversity policies encourage same-gender mentorships to retain women in academia, our findings raise the possibility that opposite-gender mentorship may actually increase the impact of women who pursue a scientific career. These findings add a new perspective to the policy debate on how to best elevate the status of women in science. 

Retracted: Yes

PubPeer comments:
 https: twitter.com millerjm86 status 1328765642372042753 , 
 https: twitter.com pollyp1 status 1329199497549918215?s=19 , 
 https: twitter.com pollyp1 status 1329455882481131524 https: twitter.com NatureComms status 1329501928062119940 , 
 https: twitter.com StatGenDan status 1330238657937207303 https: danieleweeks.github.io Mentorship #summary , 
 https: twitter.com a_succurro status 1330160359496425475?s=01 , 
 https: twitter.com eblissmoreau status 1331725285239173120 , 
 This paper got retracted in December 2020. See: https: www.nature.com articles s41467-020-20617-y  The Authors are retracting this Article in response to criticisms about the assumptions underpinning the Article in terms of the identification of mentorship relationships and the measure of mentorship quality, challenging the interpretation of the conclusions. These criticisms were raised by readers and confirmed by three experts post-publication as part of a journal-led investigation. ,
Expression and modulation of LL-37 in normal human keratinocytes, HaCaT cells, and inflammatory skin diseases
Authors: Mi Sook Jeong
Chang Kwun Hong
Seong Jun Seo
Myeung Nam Kim
Byung In Ro
Ji Eun Kim
Beom Joon Kim
Journal: Journal of Korean Medical Science (2005)
Discipline: CLINICAL MEDICINE
Keywords: Defensins; cathelicidins; antimicrobial peptides; innate immune system; skin
Affiliations: Department of Dermatology, College of Medicine, Chung Ang University, Korea., Department of Dermatology, College of Medicine, Chung Ang University, Seoul, Korea., Chung Ang Medical Research Center, Seoul, Korea.

Abstract:  Defensins and cathelicidins (LL-37) are major antimicrobial peptides (AMPs) of the innate immune system of the human skin. In normal non-inflamed skin these peptides are negligible, but their expression can be markedly increased in inflammatory skin disease such as psoriasis. We designed this study to identify the expressions of LL-37 in normal human keratinocyte (NHK) and HaCaT cells after exposure to stimulants and to investigate difference of LL-37 expression accompanied with cell differentiation status, and come to understand difference of susceptibility to infection in atopic dermatitis and psoriasis. Expressions of LL-37 in NHKs and HaCaT cells were evaluated by using RT-PCR, Western blotting, and immunohistochemical (IHC) staining at 6, 12, and 24 hr post stimulation after exposure to Ultraviolet B irradiation and lipopolysaccharide. And expression of LL-37 in skin biopsy specimens from patients with atopic dermatitis and psoriasis was determined by immunohistochemical analysis. In time-sequential analyses of LL-37 expression revealed that LL-37 was expressed in NHKs, but not in HaCaT cells. IHC analysis confirmed the presence of abundant LL-37 in the epidermis of psoriasis. Therefore we deduced that expression of LL-37 is affected by UV irradiation, bacterial infection, and status of cell differentiation. 

Retracted: No

PubPeer comments:
 Much more similar than Expected... ![file] , 
 The nature of the experiment and the related figure 6 is evident in the section heading : ** Compound 6t Failed to Induce Any Change in the p300 Structure ** This heading is clearly written in the manuscript too. The whole point of the figure 6 is to show that there was no change upon adding the 6t molecule to the native protein. The experiments were performed sequentially on the same protein sample.u00a0 that is : p300 followed by **6t added to same p300**u00a0 In fact, the figure caption also clearly mentions about resemblance. The result indicates that there is no detectable change in the Raman spectra upon addition of compound 6t. This has been clearly mentioned in the discussion related to data :  However, in the case ofu00a06t, which does not activate the p300 HAT activity, we observe that the **p300 spectrum is unaffected** or is similar to the pristine p300 (Figure 6c). ,
MicroRNA-7 regulates the proliferation and metastasis of human papillary carcinoma cells by targeting Bcl-2
Authors: Feng Zhuang
Ziwen Liu
Mengwei Wu
Xiaobin Li
Le Chang
Zhong Wang
Yimin Song
Rui Liu
Hongwei Yuan
Journal: American journal of translational research (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MicroRNA; apoptosis; flow cytometry; invasion; migration
Affiliations: Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100730, PR China., Department of General Surgery, Xinjiang Production and Construction Corps Hospital Urumqi 830002, Xinjiang, PR China.

Abstract:  Papillary carcinoma is the most common type of thyroid cancer responsible for significant number of mortalities across the globe. This study was conducted to investigate the role and therapeutic implications of microRNA-7 in human papillary carcinoma. Gene expression analysis was carried out through quantitative real time PCR method. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was performed to determine the cell proliferation. Clonogenic assay was used to assess the colony forming ability of cancer cells. Cell apoptosis was analyzed by 4',6-diamidino-2-phenylindole (DAPI), acridine orange/ethidium bromide (AO/EB) and annexin V/PI staining assays. Migration of cancer cells was estimated through scratch heal assay and cell invasion was determined by transwell assay method. Western blotting was done to examine the protein expression. Xenografted mice models were employed to examine the effects of miR-7 overexpression in vivo. Results showed miR-7 to be significantly (P &lt; 0.05) repressed in papillary carcinoma. Cancer cell proliferation was inhibited by miR-7 through induction of apoptotic cell death as revealed by DAPI, AO/EB and annexin V/PI staining assays. The colony forming potential of cancer cells also decreased under miR-7 overexpression. miR-7 overexpression also inhibited the migration and invasion of cancer cells. Bcl-2 was identified as the intracellular target of miR-7 and regulatory effects of miR-7 were seen to be exerted through translation repression of Bcl-2. The results of xenograft study revealed miR-7 overexpression significantly (P &lt; 0.05) suppressed the growth of the tumor in vivo. The results point towards the therapeutic implications of miR-7 in the management of papillary carcinoma. 

Retracted: Yes

PubPeer comments:
 Text of this review paper shows unexpected verbatim similarities to text from older papers written by other authors. Some examples of source papers are: * Mariela L. Paz et al., Cytokine 44 (2008) 70u201377, DOI: 10.1016 j.cyto.2008.06.012 * Rudiger Greinert et al. , Cancer Epidemiology 39S (2015) S75u2013S83, DOI: 10.1016 j.canep.2014.12.014 * World s Worst Places To Get A Sunburn (And How To Prevent Them) - Smarter Travel - Huffington Post 2012 * K. Kotarczak et al., European Review for Medical and Pharmacological Sciences 2015; 19: 98-112 There appear to be many other source documents as well. Maybe someone with access to plagiarism software could do an analysis? ,
Charge-transfer regulated visible light driven photocatalytic H2 production and CO2 reduction in tetrathiafulvalene based coordination polymer gel
Authors: Parul Verma
Ashish Singh
Faruk Ahamed Rahimi
Sukhendu Nath
Tapas Kumar Maji
Swapan Kumar Pati
Pallavi Sarkar
Journal: Nature Communications (2021)
Discipline: Multidisciplinary
Keywords: renewable alternatives; solar energy; hydrogen generation; CO2 reduction; metal-organic hybrid material
Affiliations: Molecular Materials Laboratory, Chemistry and Physics of Materials Unit, School of Advanced Materials (SAMat), Jawaharlal Nehru Centre for Advanced Scientific Research, Jakkur, Bangalore, 560 064, India., Theoretical Sciences Unit, School of Advanced Materials (SAMat), Jawaharlal Nehru Centre for Advanced Scientific Research, Jakkur, Bangalore, 560 064, India., Ultrafast Spectroscopy Section, Radiation & Photochemistry Division, Bhabha Atomic Research Centre, Mumbai, 400 085, India., Molecular Materials Laboratory, Chemistry and Physics of Materials Unit, School of Advanced Materials (SAMat), Jawaharlal Nehru Centre for Advanced Scientific Research, Jakkur, Bangalore, 560 064, India. .

Abstract:  The much-needed renewable alternatives to fossil fuel can be achieved efficiently and sustainably by converting solar energy to fuels via hydrogen generation from water or CO2 reduction. Herein, a soft processable metal-organic hybrid material is developed and studied for photocatalytic activity towards H2 production and CO2 reduction to CO and CH4 under visible light as well as direct sunlight irradiation. A tetrapodal low molecular weight gelator (LMWG) is synthesized by integrating tetrathiafulvalene (TTF) and terpyridine (TPY) derivatives through amide linkages and results in TPY-TTF LMWG. The TPY-TTF LMWG acts as a linker, and self-assembly of this gelator molecules with ZnII ions results in a coordination polymer gel (CPG); Zn-TPY-TTF. The Zn-TPY-TTF CPG shows high photocatalytic activity towards H2 production (530 μmol g-1h-1) and CO2 reduction to CO (438 μmol g-1h-1, selectivity &gt; 99%) regulated by charge-transfer interactions. Furthermore, in situ stabilization of Pt nanoparticles on CPG (Pt@Zn-TPY-TTF) enhances H2 evolution (14727 μmol g-1h-1). Importantly, Pt@Zn-TPY-TTF CPG produces CH4 (292 μmol g-1h-1, selectivity &gt; 97%) as CO2 reduction product instead of CO. The real-time CO2 reduction reaction is monitored by in situ DRIFT study, and the plausible mechanism is derived computationally. 

Retracted: No

PubPeer comments:
 In supplementary Figure 42, multiple regions which contain similar noise patterns under various pulse time scale. ![file] ,
Dynamic in vivo interactions among Myc network members
Authors: R M Levenson
D L Farkas
X Yin
E S Levitan
M F Landay
W Han
S C Watkins
E V Prochownik
Journal: Oncogene (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Myc oncoprotein network; c-Myc; Max; Mad proteins; GFP fusions
Affiliations: Section of Hematology/Oncology, Department of Pediatrics, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, PA 15213, USA.

Abstract:  Members of the Myc oncoprotein network (c-Myc, Max, and Mad) play important roles in proliferation, differentiation, and apoptosis. We expressed chimeric green fluorescent protein (GFP) fusions of c-Myc, Max, and three Mad proteins in fibroblasts. Individually, c-Myc and Mad proteins localized in subnuclear speckles, whereas Max assumed a homogeneous nuclear pattern. These distributions were co-dominant and dynamic, however, as each protein assumed the pattern of its heterodimeric partner when the latter was co-expressed at a higher level. Deletion mapping of two Mad members, Mad1 and Mxi1, demonstrated that the domains responsible for nuclear localization and speckling are separable. A non-speckling Mxi1 mutant was also less effective as a transcriptional repressor than wild-type Mxi1. c-Myc nuclear speckles were distinct from SC-35 domains involved in mRNA processing. However, in the presence of co-expressed Max, c-Myc, but not Mad, co-localized to a subset of SC-35 loci. These results show that Myc network proteins comprise dynamic subnuclear structures and behave co-dominantly when co-expressed with their normal heterodimerization partners. In addition, c-Myc-Max heterodimers, but not Max-Mad heterodimers, localize to foci actively engaged in pre-mRNA transcription/processing. These findings suggest novel means by which Myc network members promote transcriptional activation or repression. 

Retracted: No

PubPeer comments:
 Figure 7. Much more similar than expected. https: imgur.com zRCo6Uw , 
 2021 Editorial Expression of Concern. https: www.nature.com articles s41388-021-01953-9 The Editors-in-Chief would like to alert readers that concerns have been raised regarding this article [1]. It appears that Figure 7 contains multiple duplications. However, it does not affect the main conclusions of the article as to the subcellular location, appearance and interactions of the various proteins analysed. Richard M Levenson, Daniel L Farkas, Edward V Prochownik and Edwin S Levitan agree to this Editorial Expression of Concern. Xiao-ying Yin, Melanie F Landay, Weiping Han and Simon C Watkins have not responded to any correspondence from the publisher about this Editorial Expression of Concern. The original article can be found online at https: doi.org 10.1038 sj.onc.1204606 Reference 1. Yin X, Landay MF, Han W, Levitan ES, Watkins SC, Levenson RM, et al. Dynamic in vivo interactions among Myc network members. Oncogene. 2001;20:4650u201364. https: doi.org 10.1038 sj.onc.1204606 ,
Mammalian Prion Biology
Authors: Adriano Aguzzi
Magdalini Polymenidou
Journal: Cell (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Prions; Kuru; Creutzfeldt-Jakob disease; Bovine spongiform encephalopathy; Protein-only hypothesis

Abstract:  Prions have been responsible for an entire century of tragic episodes. Fifty years ago, kuru decimated the population of Papua New Guinea. Then, iatrogenic transmission of prions caused more than 250 cases of Creutzfeldt-Jakob disease. More recently, transmission of bovine spongiform encephalopathy to humans caused a widespread health scare. On the other hand, the biology of prions represents a fascinating and poorly understood phenomenon, which may account for more than just diseases and may represent a fundamental mechanism of crosstalk between proteins. The two decades since Stanley Prusiner's formulation of the protein-only hypothesis have witnessed spectacular advances, and yet some of the most basic questions in prion science have remained unanswered. 

Retracted: No

PubPeer comments:
 https: steamtraen.blogspot.com 2020 07 how-bad-is-self-plagiarism-case-study.html ,
Stanniocalcin-1 regulates re-epithelialization in human keratinocytes
Authors: Chris K C Wong
Bonnie H Y Yeung
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Stanniocalcin-1; re-epithelialization; wound healing; keratinocyte; migration
Affiliations: Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.

Abstract:  Stanniocalcin-1 (STC1), a glycoprotein hormone, is believed to be involved in various biological processes such as inflammation, oxidative responses and cell migration. Riding on these emerging evidences, we hypothesized that STC1 may participate in the re-epithelialization during wound healing. Re-epithelialization is a critical step that involves keratinocyte lamellipodia (e-lam) formation, followed by cell migration. In this study, staurosporine (STS) treatment induced human keratinocyte (HaCaT) e-lam formation on fibronectin matrix and migration via the activation of focal adhesion kinase (FAK), the surge of intracellular calcium level [Ca²⁺]i and the inactivation of Akt. In accompanied with these migratory features, a time- and dose-dependent increase in STC1 expression was detected. STC1 gene expression was found not the downstream target of FAK-signaling as illustrated by FAK inhibition using PF573228. The reduction of [Ca²⁺]i by BAPTA/AM blocked the STS-mediated keratinocyte migration and STC1 gene expression. Alternatively the increase of [Ca²⁺]i by ionomycin exerted promotional effect on STS-induced STC1 gene expression. The inhibition of Akt by SH6 and GSK3β by lithium chloride (LiCl) could respectively induce and inhibit the STS-mediated e-lam formation, cell migration and STC1 gene expression. The STS-mediated e-lam formation and cell migration were notably hindered or induced respectively by STC1 knockdown or overexpression. This notion was further supported by the scratched wound assay. Collectively the findings provide the first evidence that STC1 promotes re-epithelialization in wound healing. 

Retracted: No

PubPeer comments:
 Figure 4D appears to have a repeated image. *** ![file] ,
Radiation activated CHK1/MEPE pathway may contribute to microgravity-induced bone density loss
Authors: Ping Wang
Ya Wang
Xiangming Zhang
Journal: Life Sciences in Space Research (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ASARM secretion; Bone density loss; CHK1; Ionizing radiation; MEPE
Affiliations: Department of Radiation Oncology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA., Department of Radiation Oncology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA. Electronic address: .

Abstract:  Bone density loss in astronauts on long-term space missions is a chief medical concern. Microgravity in space is the major cause of bone density loss (osteopenia), and it is believed that high linear energy transfer (LET) radiation in space exacerbates microgravity-induced bone density loss; however, the mechanism remains unclear. It is known that acidic serine- and aspartate-rich motif (ASARM) as a small peptide released by matrix extracellular phosphoglycoprotein (MEPE) promotes osteopenia. We previously discovered that MEPE interacted with checkpoint kinase 1 (CHK1) to protect CHK1 from ionizing radiation promoted degradation. In this study, we addressed whether the CHK1-MEPE pathway activated by radiation contributes to the effects of microgravity on bone density loss. We examined the CHK1, MEPE and secreted MEPE/ASARM levels in irradiated (1 Gy of X-ray) and rotated cultured human osteoblast cells. The results showed that radiation activated CHK1, decreased the levels of CHK1 and MEPE in human osteoblast cells and increased the release of MEPE/ASARM. These results suggest that the radiation-activated CHK1/MEPE pathway exacerbates the effects of microgravity on bone density loss, which may provide a novel targeting factor/pathway for a future countermeasure design that could contribute to reducing osteopenia in astronauts. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than you would expect. https: imgur.com t3uNtWP , 
 Figure 3. Much more similar than you would expect. https: imgur.com 2K58pQz , 
 Figure 2. https: imgur.com RpM4vET , 
 This work is supported by grants from the National Aeronautics and Space Administration (NNX11AC30G to Y.W. and P30CA138292 to the Institute). ,
Downregulation of long non-coding RNA XIST inhibits cell proliferation, migration, invasion and EMT by regulating miR-212-3p/CBLL1 axis in non-small cell lung cancer cells
Authors: K Yang
H-Y Yu
M Liu
H-B Qiu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Non-small cell lung cancer; lncRNA XIST; miR-212-3p; CBLL1; qRT-PCR
Affiliations: Department of Oncology, The Affiliated Hospital of Hubei University of Arts and Science, Xiangyang Central Hospital, Xiangyang, Hubei, China. .

Abstract:  Objective: Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors in the world and its 5-year survival rate is very low. Long non-coding RNA X-inactive specific transcript (lncRNA XIST) has been demonstrated to play vital roles in NSCLC, but the exact molecular mechanisms underlying NSCLC still need to be further explored. Patients and methods: Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of XIST, miR-212-3p and Casitas B-lineage proto-oncogene like 1 (CBLL1). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to analyze the relationship among XIST, miR-212-3p and CBLL1. Cell Counting Kit-8 (CCK-8) assay and transwell invasion assay were carried out to evaluate cell proliferation, migration and invasion, respectively. Western blot analysis was conducted to examine the protein expression of CBLL1, E-cadherin, N-cadherin and Vimentin. Murine xenograft assay was conducted to explore the role of XIST in vivo. Results: Expression levels of XIST and CBLL1 were markedly upregulated, while the miR-212-3p level was markedly downregulated in NSCLC tissues and cells. MiR-212-3p was identified as a direct target of XIST, and miR-212-3p was predicted to target CBLL1. XIST knockdown repressed NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro, and suppressed tumor growth in vivo, while miR-212-3p inhibition restored the effects. Furthermore, CBLL1 overexpression could abolish the effects of miR-212-3p overexpression on NSCLC cell proliferation, migration, invasion and EMT in vitro. Conclusions: XIST was significantly decreased in NSCLC tissues and cells, and XIST knockdown suppressed the proliferation, migration, invasion and EMT of NSCLC cells by miR-212-3p/CBLL1 axis. These findings facilitated our understanding of lncRNA regulation in NSCLC. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected. ![file] ,
Dihydroartemisinin targets fibroblast growth factor receptor 1 (FGFR1) to inhibit interleukin 17A (IL-17A)-induced hyperproliferation and inflammation of keratinocytes
Authors: Baojiang Chen
Chen Li
Guizhen Chang
Huan Wang
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Dihydroartemisinin (DHA); IL-17A; fibroblast growth factor receptor 1 (FGFR1); psoriasis.
Affiliations: Department of Dermatology, Tianjin TEDA Hospital, Tianjin, P.R. China, Department of Internal Medicine, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, P.R. China

Abstract:  Psoriasis is a common chronic immune-mediated disease that often has a serious negative impact on the physical and mental health of patients. Dihydroartemisinin (DHA) is a drug with anti-fibrotic and anti-inflammatory effects that may be involved in the autoimmune regulation of immune diseases. However, the effects of DHA on psoriasis have not been reported comprehensively. Therefore, the aim of this study was to investigate the effect of DHA on abnormal proliferation and inflammation of epidermal keratinocyte cells in psoriasis and its mechanism of action. IL-17A-induced human epidermal keratin-forming cells (HaCaT) were used as a model. And after induction exposure to different concentrations of DHA, CCK-8, EDU staining, wound healing and Western blotting were performed to assess cell viability, proliferation, migration, differentiation and inflammatory factors, respectively. Subsequently, agonists of fibroblast growth factor receptor 1 (FGFR1) were added and the above experiments were repeated. The results showed that DHA obviously inhibited IL-17A-induced hyperproliferation, migration and expression of inflammatory factors in HaCaT cells. Furthermore, FGFR1 was highly expressed in IL-17A-induced HaCaT cells, and DHA inhibited its expression. However, the inhibitory effect of DHA on IL-17A-induced HaCaT cells was reversed after the addition of FGFR1 agonist. In conclusion, DHA could inhibit IL-17A-induced hyperproliferation and inflammation of keratinocytes by targeting FGFR1, which also provided a new target for the treatment of psoriasis. 

Retracted: No

PubPeer comments:
 This paper is full of non-scientific and odd phrases indicating that the authors are not experiences scientists. I have included a few examples. In addition, the Western immunoblots look artificial. Details regarding the Western immunoblotting method is not presented. Can the authors please provide details regarding which instrument they used to read the ECL signal? No funding is associated with this study, which is seen in almost all papers published in Issue 1 2022, Bioengineered. They are all affiliated to China. ![file] ,
Ragulator is a GEF for the rag GTPases that signal amino acid levels to mTORC1
Authors: Roberto Zoncu
David M Sabatini
Liron Bar-Peled
Lawrence D Schweitzer
Journal: Cell (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: mTOR Complex 1; mTORC1 pathway; cell growth; amino acids; RagA/B-RagC/D GTPases
Affiliations: Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology, Department of Biology, Nine Cambridge Center, Cambridge, MA 02142, USA.

Abstract:  The mTOR Complex 1 (mTORC1) pathway regulates cell growth in response to numerous cues, including amino acids, which promote mTORC1 translocation to the lysosomal surface, its site of activation. The heterodimeric RagA/B-RagC/D GTPases, the Ragulator complex that tethers the Rags to the lysosome, and the v-ATPase form a signaling system that is necessary for amino acid sensing by mTORC1. Amino acids stimulate the binding of guanosine triphosphate to RagA and RagB but the factors that regulate Rag nucleotide loading are unknown. Here, we identify HBXIP and C7orf59 as two additional Ragulator components that are required for mTORC1 activation by amino acids. The expanded Ragulator has nucleotide exchange activity toward RagA and RagB and interacts with the Rag heterodimers in an amino acid- and v-ATPase-dependent fashion. Thus, we provide mechanistic insight into how mTORC1 senses amino acids by identifying Ragulator as a guanine nucleotide exchange factor (GEF) for the Rag GTPases. 

Retracted: No

PubPeer comments:
 Fig. 1A and 1B: more similar than expected. Could the authors check? ![file] , 
 #1 I am the first author of the paper and now at the Massachusetts General Hospital Harvard Medical School. We appreciate Strobilanthes for calling this to our attention and upon checking further there does appear to have been an error during figure assembly in which these panels were used twice completely unintentionally. Attached is a figure with the corrected panels. The error does not impact any conclusion made in the figure or the paper. I have made this correction in consultation with David Sabatini. ![file] , 
 Dear authors, are you planning to issue an Erratum to correct this duplication? It s been two years since this discussion, but I cannot find any update on the official paper s landing page. ,
Sex-specific regulation of AMP-activated protein kinase (AMPK) in the Pacific oyster Crassostrea gigas
Authors: Pierre Boudry
Virgile Quillien
Jean-Yves Daniel
Eric Guévélou
Massimo Milan
Claudie Quéré
Clara E Galindo-Sánchez
Arnaud Huvet
Charlotte Corporeau
Journal: Biology of reproduction (2013)
Discipline: CLINICAL MEDICINE
Keywords: AMP-activated protein kinase; Crassostrea gigas; gametogenesis; marine bivalve; reproduction.
Affiliations: Ifremer, Laboratoire des Sciences de l'Environnement Marin (UMR 6539, LEMAR), Plouzané, France.

Abstract:  The hermaphrodite Pacific oyster Crassostrea gigas displays a high energy allocation to reproduction. We studied the expression of AMP-activated protein kinase (AMPK) during gametogenesis in the gonad and characterized the mRNA sequences of the AMPK subunits: the AMPK alpha mRNA sequence was previously characterized; we identified AMPK beta, AMPK gamma, and mRNAs of putative AMPK-related targets following bioinformatics mining on existing genomic resources. We analyzed the mRNA expression of the AMPK alpha, beta, and gamma subunits in the gonads of male and female oysters through a reproductive cycle, and we quantified the mRNA expression of genes belonging to fatty acid and glucose metabolism. AMPK alpha mRNA levels were more abundant in males at the first stage of gametogenesis, when mitotic activity and the differentiation of germinal cells occur, and were always more abundant in males than in females. Some targets of fatty acid and glucose metabolism appeared to be correlated with the expression of AMPK subunits at the mRNA level. We then analyzed the sex-specific AMPK activity by measuring the phosphorylation of the catalytic AMPK alpha protein and its expression at the protein level. Both the amount of AMPK alpha protein and threonine 172 phosphorylation appeared to be almost totally inhibited in mature female gonads at stage 3, at the time when accumulation of reserves in oocytes was promoted, while it remained at a high level in mature spermatozoa. Its activation might play a sex-dependent role in the management of energy during gametogenesis in oyster. 

Retracted: No

PubPeer comments:
 Figure 4A appears to have duplicated bands. Could the authors post uncropped originals to reassure readers? *** ![file] ,
Up-regulation of microRNA-491-5p suppresses cell proliferation and promotes apoptosis by targeting FOXP4 in human osteosarcoma
Authors: Zhixun Yin
Ming Li
Jingchen Chen
Hongmei Ding
Erxing He
Journal: Cell Proliferation (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MicroRNA-491-5p; osteosarcoma; FOXP4; proliferation; migration
Affiliations: Department of Orthopaedic Surgery, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China., Department of Anatomy, Guangzhou Medical University, Guangzhou, Guangdong, China.

Abstract:  Background and objectives: MicroRNAs are small non-coding RNAs involved in pathogenesis and progression of human malignancies. MicroRNA-491-5p (miR-491-5p) is down-regulated in many human cancers where it would serve as a tumour suppressor. However, the role played by miR-491-5p in pathogenesis of human osteosarcoma has remained largely unknown. This study has been conducted to examine effects of miR-491-5p on migration and proliferation of cells of the SAOS-2 and MG63 osteosarcoma lines, and mechanisms of those effects. Materials and methods: Levels of miR-491-5p expression in osteosarcoma tissues and in human osteosarcoma cell lines were studied using qualitative real-time polymerase chain reaction (qRT-PCR) methods. Cell viability was detected using the CCK-8 and EdU assays, while the transwell assay was used to evaluate migration and invasion. Apoptosis was analysed uing flow cytometry and the Hoechst 33342 nuclear staining method. A dual-luciferase reporter system was used to confirm the target gene of miR-491-5p. The electrophoretic mobility shift assay (EMSA) with DIG-labelled double-stranded FOXP4 oligonucleotides was used to confirm whether or not miR-491-5p suppressed FOXP4 activation. Results: Cells of osteosarcoma tissues and cell lines had low levels of miR-491-5p expression, but high levels of forkhead-box P4 (FOXP4) expression. Transfection of SAOS-2 and MG63 cells with miR-491-5p mimics inhibited expression of FOXP4 protein, which suppressed cell growth and migration, but induced apoptosis. Dual-luciferase reporter assays confirmed FOXP4 as the target gene for miR-491-5p. Overexpression of miR-491-5p suppressed FOXP4 activity in SAOS-2 and MG63 cells. Knockdown of FOXP4 in SAOS-2 and MG63 cells using an RNAi strategy resulted in reduced levels of cell proliferation and migration, but increased levels of apoptosis. Conclusion: Our in vitro studies showed that up-regulation of miR-491-5p suppressed proliferation of the human osteosarcoma cells and induced apoptosis by targeting FOXP4. These findings suggest that miR-491-5p could be further studied as a potential clinical diagnostic or predictive biomarker for human osteosarcoma. 

Retracted: No

PubPeer comments:
 Images in figure 3A and 8A are entirely the same. It s the same cell line, but at the very least the treated cells should be different: ![file] ![file] , 
 An update: there are more trouble with this article. A micrograph has been duplicated and presented as something else, in Figure 3 and 8. ![file] ,