PReD-Bench/PRed-Bench huggingface dataset:
Overexpression of RKIP inhibits cell invasion in glioma cell lines through upregulation of miR-98
Authors: Renjun Peng
Zigui Chen
Haipeng Xi
Zhiming Ma
Quan Cheng
Bing Jiang
Journal: BioMed research international (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RKIP; miR-98; glioma; invasion; metastasis
Affiliations: Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Abstract:  Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor in cancer cells. MicroRNAs (miRNAs) have been suggested to play a vital role in tumor initiation and progression by negatively regulating oncogenes and tumor suppressors. Quite recently, studies have identified some miRNAs operating to promote or suppress tumor invasion or metastasis via regulating metastasis-related genes, providing potential therapeutic targets on antimetastasis strategy. In this study, we found that the expression of RKIP and miR-98 in glioma tissues were significantly lower than that in normal brain tissues. Overexpression of RKIP upregulated miR-98 expression and inhibited glioma cell invasion and miR-98 target gene HMGA2 but had no effect in glioma cell proliferation. Moreover, forced expression of miR-98 accelerated the inhibition of glioma cell invasion and the expression of HMGA2 also had no effect in glioma cell proliferation. Our findings newly described RKIP/miR-98 to HMGA2 link and provided a potential mechanism for glioma cell invasion. RKIP and miR-98 may illustrate the potential therapeutic utility of signaling pathway signatures. 

Retracted: No

PubPeer comments:
null, 
 2018 retraction. http: iai.asm.org content 86 6 e00212-18 RETRACTION Volume 77, no. 3, p. 1031u20131043, 2009, https: doi.org 10.1128 IAI.01192-08. The publisher hereby retracts this article. Questions have been raised by concerned readers about the integrity of the data. The American Society for Microbiology has reviewed the figures and confirmed evidence of apparent duplication of cell images and Western blot bands in Fig. 1C, 2D, 5A, and 5B. Since the integrity of the data as presented was compromised, this publication is retracted in its entirety. We apologize to the readers of Infection and Immunity and regret any inconvenience that this causes. , 
 Here are the concerns as communicated with the journal in March of 2015. ![file] , 
 Two recent Retraction Watch articles and an ORI report about this case: * Infectious disease researcher u201crecklesslyu201d faked data in grants worth millions, says federal watchdog - https: retractionwatch.com 2020 07 21 infectious-disease-researcher-recklessly-faked-data-in-grants-worth-millions-says-federal-watchdog * USC-Childrenu2019s Hospital Los Angeles researcher out following misconduct probe - https: retractionwatch.com 2020 07 29 usc-childrens-hospital-los-angeles-researcher-out-following-misconduct-probe * Case Summary: Nemani, Prasadarao - https: ori.hhs.gov content case-summary-nemani-prasadarao ,
Mitochondrial Metabolism Regulates Microtubule Acetylome and Autophagy Trough Sirtuin-2: Impact for Parkinson’s Disease
Authors: Ana R Esteves
Diana F Silva
Sofia D Viana
Frederico C Pereira
Sandra M Cardoso
Daniela M Arduíno
Journal: Molecular neurobiology (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Macroautophagy; Microtubule acetylation; Mitochondrial metabolism; Sirtuin-2.
Affiliations: CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517, Coimbra, Portugal., CNC-IBILI, Coimbra, Portugal., Pharmacy Department/Coimbra Health School, Polythecnic Institute of Coimbra, Coimbra, Portugal., Laboratory of Pharmacology and Experimental Therapeutics/IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal., CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517, Coimbra, Portugal. ., CNC-IBILI, Coimbra, Portugal. ., Institute of Cellular and Molecular Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal. .

Abstract:  Alterations in microtubule-dependent transport, mitochondrial dysfunction, and autophagic pathology are involved in neurodegeneration observed in sporadic Parkinson's disease. However, the mechanistic link connecting these events remains elusive. We observed that NAD+ metabolism is altered in sporadic Parkinson's disease patient-derived cells, which contributes to Sirtuin-2 activation and subsequent decrease in acetylated-α-tubulin levels. Pharmacological inhibition of sirtuin-2 deacetylase activity selectively enhanced α-tubulin acetylation and facilitated the trafficking and clearance of misfolded proteins. Sirtuin-2 knock-out mice neurons had no alteration in microtubule assembly after exposure to MPP+, allowing the maintenance of a normal autophagic flux. These data were validated using MPTP-treated sirtuin-2 knock-out mice, where no alterations in motor behavior were observed. Biochemical analysis of sporadic Parkinson's disease patient brains supports the in vitro and in vivo data. Our data provide strong evidence that sirtuin-2 controls the functional ability of the autophagic system through acetylation and highlight the association between mitochondrial metabolism and neurodegeneration in sporadic Parkinson's disease. 

Retracted: No

PubPeer comments:
 Figure one appears to have a repeated image. *** Closeup ![file] *** Full figure ![file] , 
 February 2, 2021  Following publication of the original article [1], the authors (sic) identified an unintended error in the Fig. 1c. The picture of EV71 (ZZ1350)-induced CPE in Vero cells at the MOI of 5.0 was the same for the picture of EV71 (ZZ1350)-induced CPE in Vero cells at the MOI of 1.0. These two pictures were captured under different backgrounds and were mistakenly put together during submission. In this Correction, the picture of EV71 (ZZ1350)-induced CPE in Vero cells at the MOI of 5.0 has now been replaced with the correct picture. We are sorry for the inconvenience caused by this unintended error. This correction does not affect the results and conclusions of this work. ![file] ,
Toll-like receptor 2 signaling in CD4(+) T lymphocytes promotes T helper 17 responses and regulates the pathogenesis of autoimmune disease
Authors: Chen Dong
Qiang Tian
Bhanu P Pappu
Gustavo J Martinez
Juan Peng
Xuexian O Yang
Roza I Nurieva
Joseph M Reynolds
Yongliang Zhang
Li Ma
Yeonseok Chung
Journal: Immunity (2010)
Discipline: IMMUNOLOGY
Keywords: Toll-like receptors; TLR2; T helper 17; Th17 cell responses; innate immunity
Affiliations: Department of Immunology and Center for Inflammation and Cancer, M.D. Anderson Cancer Center, Houston, TX 77054, USA.

Abstract:  Toll-like receptors (TLRs) have previously been shown to play critical roles in the activation of innate immunity. Here, we describe that T cell expression of TLR2 regulates T helper 17 (Th17) cell responses. Stimulation with TLR2 agonists promoted Th17 differentiation in vitro and led to more robust proliferation and Th17 cytokine production. Using the experimental autoimmune encephalomyelitis (EAE) model, we found that TLR2 regulated Th17 cell-mediated autoimmunity in vivo and that loss of TLR2 in CD4(+) T cells dramatically ameliorated EAE. This study thus reveals a critical role of a TLR in the direct regulation of adaptive immune response and pathogenesis of autoimmune diseases. 

Retracted: No

PubPeer comments:
 Figure 4C showed identical images for WT Pam3Cys and Pam3+IL-23. Please explain. ![file] , 
 In this experiment, we analyzed the effect of TLR2 ligation on T cell proliferation by incubating them with various stimuli overnight prior to proliferation assessment by CFSE dye division. The result showed that there was no additional effect on T cell proliferation when IL-23 was added in combination with Pam3, a TLR2 ligand. While the 2 figures look similar, which is expected given the similar amounts of cell proliferation and the nature of histograms, it remains possible that the images were erroneously duplicated during figure preparation. Unfortunately, these experiments were run 11-12 years ago and the original Cell Quest Pro analysis files cannot be found (both the first and corresponding have moved to different institutions and no longer have access to data on core facility computers). However, we were able to find raw data that may represent the original data, or, at the very least, the replicates of similar experiments. As shown in the picture, IL-23 clearly had no proliferative effect by itself or in conjunction with Pam3, which is the very same conclusion in the paper. We are contacting the journal to obtain their advice on this situation and on whether a figure replacement is needed. -Joseph Reynolds and Chen Dong ![file] ,
MEPE/OF45 protects cells from DNA damage induced killing via stabilizing CHK1
Authors: Shuang Liu
Peter S N Rowe
Lin Lu
Ya Wang
Ning Gao
Xiang Wang
Baocheng Hu
Hongyan Wang
Journal: Nucleic acids research (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MEPE/OF45; CHK1; DNA damage; ionizing radiation; camptothecin
Affiliations: Beijing Institute of Biotechnology, Beijing 100850, China.

Abstract:  Matrix extracellular phosphoglycoprotein/osteoblast factor 45 (MEPE/OF45) was cloned in 2000 with functions related to bone metabolism. We identified MEPE/OF45 for the first time as a new co-factor of CHK1 in mammalian cells to protect cells from DNA damage induced killing. We demonstrate here that MEPE/OF45 directly interacts with CHK1. Knocking down MEPE/OF45 decreases CHK1 levels and sensitizes the cells to DNA damage inducers such as ionizing radiation (IR) or camptothicin (CPT)-induced killing. Over-expressing wild-type MEPE/OF45, but not the mutant MEPE/OF45 (depleted the key domain to interact with CHK1) increases CHK1 levels in the cells and increases the resistance of the cells to IR or CPT. MEPE/OF45, interacting with CHK1, increases CHK1 half-life and decreases CHK1 degradation through the ubiquitine-mediated pathway. In addition, the interaction of MEPE/OF45 with CHK1 decreases CHK1 levels in the ubiquitin E3 ligases (Cul1 and Cul4A) complex, which suggests that MEPE/OF45 competes with the ubiquitin E3 ligases binding to CHK1 and thus decreases CHK1 from ubiquitin-mediated proteolysis. These findings reveal an important role of MEPE/OF45 in protecting cells from DNA damage induced killing through stabilizing CHK1, which would provide MEPE/OF45 as a new target for sensitizing tumor cells to radiotherapy or chemotherapy. 

Retracted: Yes

PubPeer comments:
 Figure 1A. Much more similar than you would expect. https: imgur.com dUs5gAM , 
 Figure 4A. Much more similar than you would expect. https: imgur.com LnSOBlj , 
 31 March 2022 retraction. https: academic.oup.com nar advance-article doi 10.1093 nar gkac211 6555424 In September 2021, a reader raised concerns about PCNA and CHK-1 Western-blot bands in Figures 1A and 4A, respectively. While the institution found insufficient evidence to move forward with an investigation in 2020, a detailed examination of the figures by the editors found evidence of inappropriate image manipulation. A consultant subsequently hired by the institution corroborated the findings. There may be additional issues beyond the ones reported here. Collectively, these issues render the findings unreliable, and the conclusions may no longer be valid. The authors are also unable to provide the original data for inspection. The Editors are, therefore, retracting the article. , 
 https: ori.hhs.gov content case-summary-wang-ya ,
Acute Fasting Does Not Induce Cognitive Impairment in Mice
Authors: Hua Zheng
Zhongcong Xie
Lei Yang
Hoai Ton
Yiying Zhang
Ning Liufu
Yuanlin Dong
Journal: Frontiers in neuroscience (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: acute fasting; cellular apoptosis; cognitive impairment; mice; neural activation.
Affiliations: Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China., Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United States.

Abstract:  Preoperative baseline cognitive impairment is associated with postoperative neurocognitive disorder (PND). Fasting, and more generally, calorie restriction has been shown to exert controversial effects in clinical settings and various animal models of neurological disorders. Every patient needs acute fasting before anesthesia and surgery. However, the impact of acute fasting on cognitive function remain largely unknown. We, therefore, set out to determine whether acute fasting can induce neurotoxicity and neurobehavioral deficits in rodents. In the present system establishment study, a mouse model of acute fasting was established. The effects of the acute fasting on natural and learned behavior were evaluated in the buried food test, open field test and the Y maze test. The expression of c-Fos, the marker of neuronal activation, and caspase-3 activation, the marker of cellular apoptosis, were measured with immunohistochemistry. We found that the 9 h acute fasting increased the latency to eat food in the buried food test. The acute fasting also selectively increased the total distance and decreased the freezing time in open field test, and increased the duration in the novel arm in the Y maze test. Besides, the immunohistochemical study showed that the fasting significantly increased the c-Fos level in the hippocampus and various sub-cortical areas, including paraventricular thalamus (PVT), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), and basal amygdala (BMA). However, the acute fasting did not induce apoptosis, demonstrating by no appearance of caspase-3 activation in the corresponding brain areas. These data showed that acute fasting did not cause cellular apoptosis and cognitive impairment in the mice. Instead, the acute fasting increased the neuronal activity, enhanced the ambulatory activity and improved the spatial recognition memory in the mice. These findings will promote more research in the established system to further determine the effects of perioperative factors on the postoperative neurocognitive function and the underlying mechanisms. 

Retracted: No

PubPeer comments:
 more similar than expected in figure 5. an arrow shows picture chopped. ![file] , 
 similar shape of DG angle in control and fasting group ![file] , 
 similar shape of DG angle in control and fasting group (figure 7). ![file] ,
Do sounds near the hand facilitate tactile reaction times? Four experiments and a meta-analysis provide mixed support and suggest a small effect size
Authors: William Mitchell
Dennis Martin
Zeeshan Noorani
Amber Thorne
Nicholas Paul Holmes
Journal: Experimental Brain Research (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Audition; Go/NoGo; Multisensory; Reaction time; Touch
Affiliations: School of Psychology, University of Nottingham, Nottingham, NG7 2RD, UK. ., School of Psychology and Clinical Language Sciences, University of Reading, Reading, RG6 6AL, UK.

Abstract:  The brain represents the space immediately surrounding the body differently to more distant parts of space. Direct evidence for this 'peripersonal space' representation comes from neurophysiological studies in monkeys, which show distance-dependent responses to visual stimuli in neurons with spatially coincident tactile responses. Most evidence for peripersonal space in humans is indirect: spatial- and distance-dependent modulations of reaction times and error rates in behavioural tasks. In one task often used to assess peripersonal space, sounds near the body have been argued to speed reactions to tactile stimuli. We conducted four experiments attempting to measure this distance-dependent audiotactile interaction. We found no distance-dependent enhancement of tactile processing in error rates or task performance, but found some evidence for a general speeding of reaction times by 9.5 ms when sounds were presented near the hand. A systematic review revealed an overestimation of reported effect sizes, lack of control conditions, a wide variety of methods, post hoc removal of data, and flexible methods of data analysis. After correcting for the speed of sound, removing biased or inconclusive studies, correcting for temporal expectancy, and using the trim-and-fill method to correct for publication bias, meta-analysis revealed an overall benefit of 15.2 ms when tactile stimuli are accompanied by near sounds compared to sounds further away. While this effect may be due to peripersonal space, response probability and the number of trials per condition explained significant proportions of variance in this near versus far benefit. These confounds need to be addressed, and alternative explanations ruled out by future, ideally pre-registered, studies. 

Retracted: No

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: A 5-expt (failure of) replication, we over-relied on *reported* methods didn t get the experiment working properly before testing the hypothesis. This is more a running commentary than the strongest possible test. I won t be going back to it as I never believed the effect was real anyway. Prove me wrong! ,
Hepatocyte IKKbeta/NF-kappaB inhibits tumor promotion and progression by preventing oxidative stress-driven STAT3 activation
Authors: Markus Peck-Radosavljevic
Michael Karin
Christian Kuntzen
Guobin He
Vladislav Temkin
Hyam L Leffert
Hisanobu Ogata
Toshiharu Sakurai
Wolfgang Sieghart
Guann-Yi Yu
Journal: Cancer Cell (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: IKKbeta; liver tumorigenesis; hepatocellular carcinomas; HCC development; tumor initiating cells
Affiliations: Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.

Abstract:  The NF-kappaB activating kinase IKKbeta suppresses early chemically induced liver tumorigenesis by inhibiting hepatocyte death and compensatory proliferation. To study IKKbeta's role in late tumor promotion and progression, we developed a transplant system that allows initiated mouse hepatocytes to form hepatocellular carcinomas (HCC) in host liver after a long latency. Deletion of IKKbeta long after initiation accelerated HCC development and enhanced proliferation of tumor initiating cells. These effects of IKKbeta/NF-kappaB were cell autonomous and correlated with increased accumulation of reactive oxygen species that led to JNK and STAT3 activation. Hepatocyte-specific STAT3 ablation prevented HCC development. The negative crosstalk between NF-kappaB and STAT3, which is also evident in human HCC, is a critical regulator of liver cancer development and progression. 

Retracted: No

PubPeer comments:
 Identified by another reader. See also https: retractionwatch.com 2012 08 29 authors-including-highly-cited-cancer-researcher-blame-clerical-error-for-image-mixup-in-cancer-paper *** ![file] ,
L-dopa methyl ester attenuates amblyopia-induced neuronal injury in visual cortex of amblyopic cat
Authors: Rong Li
Xing Lin
Shijun Zhang
Tao Liang
Zhaoni Chen
Renbin Huang
Journal: Gene (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 3,4-dihydroxyphenylacetic acid; ANOVA; AP-1; Amblyopia; BBB
Affiliations: Department of Pharmacology, Guangxi Medical University, Nanning, Guangxi 530021, PR China.

Abstract:  In the present study, we aimed to assess the potential anti-amblyopic effects of L-dopa methyl ester (LDME) on visual cortex area 17 in an amblyopic feline model induced by monocular vision deprivation. After LDME administration, pathophysiologic and ultrastructural observations were utilized to examine the morphological changes of nerve cells in visual cortex area 17. Dopamine (DA) and its metabolite contents in visual cortex area 17 were investigated through HPLC analysis. Apoptotic cells in visual cortex area 17 were evaluated by TUNEL assay. Additionally, the c-fos expression both at gene and protein levels was assessed using RT-PCR and immunohistochemistry analyses, respectively. The contents of DA and its metabolites were elevated in visual cortex area 17. Neuronal rejuvenation which occurred in visual cortex area 17 was observed through anatomical and physiological assessments. Similarly, TUNEL results showed that neuronal apoptosis was inhibited in the visual cortex of amblyopic cats by both L-dopa and LDME therapies. Meanwhile, the c-fos expression was notably up-regulated at both the mRNA and protein levels by the treatments. These findings suggested that LDME treatment could effectively increase DA and its metabolite contents, and restrain the apoptotic process, as well as elevate the c-fos expression in nerve cells of visual cortex area 17. Taken together, LDME might ameliorate the functional cytoarchitecture in visual cortex area 17 through mechanisms that elevate DA content and increase endogenous c-fos expression, as well as inhibit neuronal lesion in visual cortex tissue. 

Retracted: No

PubPeer comments:
 Figure 5. A and E seem to have an overlap, though they represent different experimental groups of animals. ![file] , 
 #1 Dear Dr Oeneis Buddha, We appreciate your kind work for finding our manuscript mistake in two figure presentations. We re-check our raw data and sorry to make this mistake figure use due to our carelessness. And we will make a corrigendum in Gene journal ASAP. Once again, we thank for your helpful effort for our research improvement. Best regards, Prof RB Huang , 
 Corrigendum [20 April 2021] . ------------------------------- The authors regret to misuse the Nissl-staining images in Fig. 3A and E in the manuscript. We checked all the raw data and then correct the figure by use of this revised Fig. 3. ![] ,
Interactions between syntaxins identify at least five SNARE complexes within the Golgi/prevacuolar system of the Arabidopsis cell
Authors: V Kovaleva
D C Bassham
A A Sanderfoot
N V Raikhel
Journal: Molecular Biology of the Cell (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Syntaxin; SNAREs; Arabidopsis thaliana; gene families; SYPs
Affiliations: Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI 48824-1312, USA., Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824-1312; and, Department of Biochemistry, Michigan State University, East Lansing, Michigan 48824-1319

Abstract:  The syntaxin family of soluble N-ethyl maleimide sensitive factor adaptor protein receptors (SNAREs) is known to play an important role in the fusion of transport vesicles with specific organelles. Twenty-four syntaxins are encoded in the genome of the model plant Arabidopsis thaliana. These 24 genes are found in 10 gene families and have been reclassified as syntaxins of plants (SYPs). Some of these gene families have been previously characterized, with the SYP2-type syntaxins being found in the prevacuolar compartment (PVC) and the SYP4-type syntaxins on the trans-Golgi network (TGN). Here we report on two previously uncharacterized syntaxin groups. The SYP5 group is encoded by a two-member gene family, whereas SYP61 is a single gene. Both types of syntaxins are localized to multiple compartments of the endomembrane system, including the TGN and the PVC. These two groups of syntaxins form SNARE complexes with each other, and with other Arabidopsis SNAREs. On the TGN, SYP61 forms complexes with the SNARE VTI12 and either SYP41 or SYP42. SYP51 and SYP61 interact with each other and with VTI12, most likely also on the TGN. On the PVC, a SYP5-type syntaxin interacts specifically with a SYP2-type syntaxin, as well as the SNARE VTI11, forming a SNARE complex likely involved in TGN-to-PVC trafficking. 

Retracted: No

PubPeer comments:
 The edible portion of the radish is a root, rather than a tuber. ,
Children are unlikely to be the main drivers of the COVID‐19 pandemic – A systematic review
Authors: Jonas F Ludvigsson
Journal: Acta Paediatrica (2020)
Discipline: CLINICAL MEDICINE
Keywords: COVID-19; children; coronavirus; pandemic; transmission.
Affiliations: Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden., Department of Paediatrics, Orebro University Hospital, Orebro, Sweden., Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK., Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA.

Abstract:  Aim: Many countries have closed schools and kindergartens to minimise COVID-19, but the role that children play in disease transmission is unclear. Methods: A systematic literature review of the MEDLINE and EMBASE databases and medRxiv/bioRxiv preprint servers to 11 May 2020 identified published and unpublished papers on COVID-19 transmission by children. Results: We identified 700 scientific papers and letters and 47 full texts were studied in detail. Children accounted for a small fraction of COVID-19 cases and mostly had social contacts with peers or parents, rather than older people at risk of severe disease. Data on viral loads were scarce, but indicated that children may have lower levels than adults, partly because they often have fewer symptoms, and this should decrease the transmission risk. Household transmission studies showed that children were rarely the index case and case studies suggested that children with COVID-19 seldom caused outbreaks. However, it is highly likely that children can transmit the SARS-COV-2 virus, which causes COVID-19, and even asymptomatic children can have viral loads. Conclusion: Children are unlikely to be the main drivers of the pandemic. Opening up schools and kindergartens is unlikely to impact COVID-19 mortality rates in older people. 

Retracted: No

PubPeer comments:
 The abstract of this paper begins with the statement  *New efficient nonlinear optical (NLO) organic single crystals of quinoline 4-nitrophenol (QNP) were grown by slow evaporation solution technique (SEST) at room temperature using methanol as solvent.*  In the single crystal X-ray study it is noted that this novel NLO material crystallized in the centrosymmetric space group P21 c space group. It is not clear if the structure determination especailly the space group is incorrect. It is also not clear how such a crystal can be useful NLO applications as given in the title. Authors are requested to clarify this. ,
BMP9 promotes osteogenic differentiation of SMSCs by activating the JNK/Smad2/3 signaling pathway
Authors: Yu Zhang
Qian Chen
Weiwei Zheng
Zepeng Yu
Yuefeng Hao
Xueping Gu
Rui Xia
Dan Hu
Xingwei Sun
Journal: Journal of Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: bone formation; bone morphogenetic protein 9; osteogenic differentiation; synovial mesenchymal stem cells.
Affiliations: Department of Orthopaedics, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, China., Laboratory Center, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, China., Department of Orthopaedics, The Second Affiliated Hospital of Soochow University, Suzhou, China., Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China., Department of Intervention, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Abstract:  Synovial mesenchymal stem cells (SMSCs) with high proliferation and multi differentiation ability, and low immunogenicity have attracted research attention for their potential application in tissue engineering. Once their ability of osteogenesis is strengthened, it will be of practical value to apply the SMSCs in the field of bone regeneration. The current study aimed to investigate the osteogenic characteristics of SMSCs induced by bone morphogenetic protein 9 (BMP9) both in vitro and in vivo and to elucidate the mechanism underlying these characteristics. Specifically, different BMPs were assessed to determine the protein that would be the most favorable for stimulating osteogenic differentiation of SMSCs following their separation. The BMP9-enhanced osteogenesis of SMSCs was fully investigated in vitro and in vivo, and the c-Jun N-terminal kinase (JNK)/Smad2/3 signaling pathway stimulated by BMP9 was further explored. Our data suggested that BMP9 could significantly promote gene and protein expression of runt-related transcription factor 2, alkaline phosphatase, osteopontin, and osteocalcin, and SP600125, a JNK-specific inhibitor, could effectively decrease this tendency. Similar results were also confirmed in rats with cranial defects. In conclusion, our study indicated that BMP9 promotes bone formation both in vitro and in vivo possibly by activating the JNK/Smad2/3 signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 3A. * Yellow boxes: The MOI40 and MOI80 panels appear to show an overlap. Of note, they also differ in intensity. ![file] ,
Downregulation of microRNA-138 enhances the proliferation, migration and invasion of cholangiocarcinoma cells through the upregulation of RhoC/p-ERK/MMP-2/MMP-9
Authors: Shanshan Yin
Chao Dong
Qi Wang
Huihuan Tang
Journal: Oncology reports (2013)
Discipline: CLINICAL MEDICINE
Keywords: microRNAs; miR-138; cholangiocarcinoma; RhoC; proliferation
Affiliations: Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China.

Abstract:  microRNAs (miRs) play an important role in tumor initiation and progression in many types of cancer, including cholangiocarcinoma (CC). miR-138 dysregulation is frequently observed in a variety of tumors. In the present study, miR-138 was found to be downregulated in CC tissues by quantitative real-time RT-PCR. Furthermore, its potential target molecule, Ras homolog gene family, member C (RhoC) protein, was found to be highly expressed in CC tissues examined by western blot analysis. Luciferase reporter assay further demonstrated that miR-138 directly targeted RhoC. We found that the introduction of miR-138 mimics to RBE and QBC939 CC cells could reduced RhoC mRNA and protein expression, and suppressed the proliferation, G1/S transition, migration and invasion of CC cells. However, transfection with a miR-138 inhibitor induced an inverse effect in CC cells. The expression of phosphorylated extracellular signal-regulated kinase (p-ERK), matrix metalloproteinase (MMP)-2 and MMP-9 decreased following transfection with miR-138, and increased following transfection with miR-138 inhibitor in CC cells. In conclusion, RhoC upregulation induced by miR-138 downregulation promotes the malignant progression of CC cells and the underlying mechanisms of this effect involve the increase in the expression of p-ERK/MMP-2/MMP-9. Consequently, miR-138/RhoC is a potential target for the clinical diagnosis and treatment of CC. 

Retracted: No

PubPeer comments:
 Fig 3.  Effects of miR-138 RhoC on cell viability and cell cycle distribution. The cholangiocarcinoma cells were transfected with miR-138 mimics, miR-138 inhibtor (inhibitor) or negative control (NC) of miR-138 . ![file] Coloured rectangles refer to the re-appearance of the same panels in Fig 3 of [Chen et al (2016)] ,  B16 and A375 cells were transfected with miR-NC or miR-18b mimic, respectively. (A and B) Cell cycle distribution was determined using flow cytometry . ![file] Fig 4A of [Li et al (2014)] ,  miR-22 inhibited E2-induced cell cycle progression in RL95-2 and Ishikawa cells. (A) Cell cycle assay was performed to investigate the effect of miR-22 on E2-induced cell cycle progression in RL95-2 and Ishikawa cells. ![file] Fig 3 of [Liu et al (2016)] . ![file] ,
T cell receptor-mediated activation of CD4+CD44hi T cells bypasses Bcl10: an implication of differential NF-kappaB dependence of naïve and memory T cells during T cell receptor-mediated responses
Authors: Renren Wen
Yuhong Chen
Hu Zeng
Demin Wang
Stephan W Morris
Xiang Gao
Mei Yu
Liquan Xue
Journal: Journal of Biological Chemistry (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bcl10; T cell activation; CD44; IL2 production; proliferation
Affiliations: Model Animal Research Center, State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 225001, China.

Abstract:  Previous studies have demonstrated that Bcl10 (B-cell leukemia/lymphoma 10) is essential for T cell receptor-mediated NF-kappaB activation and subsequent proliferation and interleukin 2 (IL2) production. However, here we demonstrate that, contrary to expectations, Bcl10 is differentially required for T cell activation, including for both proliferation and cytokine production. When CD4+ and CD8+ T cells were divided based on expression levels of CD44, which distinguishes naïve cells (CD44lo) versus those that are antigen-experienced (CD44hi), IL2 production by and proliferation of CD4+CD44lo naïve cells and both subpopulations of CD8+ T cells were clearly Bcl10-dependent, whereas these same functional properties of CD4+CD44hi T cells occurred largely independent of Bcl10. As with the other subpopulations of T cells, CD4+CD44hi T cells did not activate the NF-kappaB pathway in the absence of Bcl10; nevertheless, these CD4+CD44hi antigen-experienced T cells efficiently secreted IL2 after T cell receptor stimulation. Strikingly, therefore, T cell receptor-mediated IL2 production in these cells is NF-kappaB-independent. Our studies suggest that antigen-experienced CD4+ T cells differ from their naïve counterparts and from CD8+ T cells in their ability to achieve activation independent of the Bcl10/NF-kappaB pathway. 

Retracted: No

PubPeer comments:
 ![file] ,
Effectiveness of Virtual Reality on Functional Performance after Spinal Cord Injury: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
Authors: David Lucena-Anton
M Dolores Rubio
Rocio Camacho
Alejandro Salazar
Amaranta De Miguel-Rubio
Journal: Journal of Clinical Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: functional performance; neurological rehabilitation; physical therapy; quality of life; spinal cord injuries
Affiliations: Department of Nursing, Pharmacology and Physiotherapy, University of Cordoba, 14004 Cordoba, Spain., Department of Cell Biology, Physiology, and Immunology, University of Cordoba, 14007 Cordoba, Spain., Department of Statistics and Operational Research, University of Cadiz, 11009 Cadiz, Spain., Institute of Research and Innovation in Biomedical Sciences of the Province of Cadiz (INiBICA), University of Cadiz, 11009 Cadiz, Spain., The Observatory of Pain, University of Cadiz, 11009 Cadiz, Spain., Department of Nursing and Physiotherapy, University of Cadiz, 11009 Cadiz, Spain.

Abstract:  A spinal cord injury (SCI) usually results in a significant limitation in the functional outcomes, implying a challenge to the performance of activities of daily living. The main aim of this study is to analyze the effectiveness of virtual reality to improve functional performance in patients with SCI. The search was performed between October and December 2019 in Cumulative Index to Nursing and Allied Health Literature (CINAHL), Medline, Cochrane Central Register of Controlled Trials, Physiotherapy Evidence Database (PEDro), PubMed, Scopus, Web of Science, and Embase. The methodological quality of the studies was evaluated through the PEDro scale, and the risk of bias was evaluated with the Cochrane collaboration's tool. Seven articles were included in this systematic review, and five of them in the meta-analysis. Statistical analysis showed favorable results for functional performance in control group performing conventional therapy, measured by the functional independence measure (standardized mean difference (SMD)= -0.70; 95% confidence interval: -1.25 to -0.15). Results were inconclusive for other outcomes. Most studies have not shown beneficial effects on functional performance compared with conventional physical therapy. The results obtained showed that virtual reality may not be more effective than conventional physical therapy in improving functional performance in patients with SCI. 

Retracted: No

PubPeer comments:
 Correspond authors of these works should explain the similarities of the two. **Is Virtual Reality Effective for Balance Recovery in Patients with Spinal Cord Injury? A Systematic Review and Meta-Analysis ** [](http: ) https: www.mdpi.com 2077-0383 9 9 2861 Seems they are introducing ghost authors in the second review. ,
Characterization of phosphoglycerate kinase-1 expression of stromal cells derived from tumor microenvironment in prostate cancer progression
Authors: Jian Lu
Jingchen Wang
Younghun Jung
Gigi Ying
Russell S Taichman
Jianhua Wang
Kenneth J Pienta
Jiang Zhu
Journal: Cancer Research (2010)
Discipline: CLINICAL MEDICINE
Keywords: Tumor-stromal interactions; Prostate cancer; Cancer-associated fibroblasts (CAF); Phosphoglycerate kinase-1 (PGK1); Glycolytic pathway
Affiliations: Institute of Medical Sciences, Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, PR. China. 

Abstract:  Tumor and stromal interactions in the tumor microenvironment are critical for oncogenesis and cancer progression. Our understanding of the molecular events by which reactive stromal fibroblasts-myofibroblast or cancer-associated fibroblasts (CAF)-affect the growth and invasion of prostate cancer remains unclear. Laser capture microdissection and cDNA microarray analysis of CAFs in prostate tumors revealed strong upregulation of phosphoglycerate kinase-1 (PGK1), an ATP-generating glycolytic enzyme that forms part of the glycolytic pathway and is directly involved in CXCL12-CXCR4 signaling. Normal fibroblasts overexpressing PGK1 resembled myofibroblasts in their expression of smooth muscle alpha-actin, vimentin, and high levels of CXCL12. These cells also displayed a higher proliferative index and the capability to contribute to prostate tumor cell invasion in vitro, possibly through expression of MMP-2 and MMP-3 and activation of the AKT and ERK pathways. Coimplantation of PGK1-overexpressing fibroblasts with prostate tumor cells promoted tumor cell growth in vivo. Collectively, these observations suggest that PGK1 helps support the interactions between cancer and its microenvironment. 

Retracted: No

PubPeer comments:
 Same images in fig.4k and fig.4n ,
miR-21 deficiency inhibits osteoclast function and prevents bone loss in mice
Authors: Bing-Dong Sui
Yi Shuai
Fang-Ying Du
Cheng-Hu Hu
Chen-Xi Zheng
Pan Zhao
Xiao-Rui Yu
Yan Jin
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: MicroRNAs; bone metabolism; miR-21; osteogenesis; osteoclastogenesis
Affiliations: Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, China., State Key Laboratory of Military Stomatology &National Clinical Research Center for Oral Diseases &Shaanxi International Joint Research Center for Oral Diseases, Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Shaanxi 710032, China., Xi'an Institute of Tissue Engineering and Regenerative Medicine, Xi'an, Shaanxi 710032, China.

Abstract:  MicroRNAs emerge as critical post-transcriptional regulators in bone metabolism. We have previously reported in vitro that miR-21 promotes osteogenesis, while studies have also revealed miR-21 as a regulator of osteoclastogenesis and a promoter of osteoclast differentiation in vitro. However, in vivo data are still lacking in identifying skeletal function of miR-21, particularly its effects on osteoporosis. Here, using miR-21 knockout (miR-21-/-) mice, we investigated effects of miR-21 on bone development, bone remodeling and bone loss. Unexpectedly, miR-21-/- mice demonstrated normal skeletal phenotype in development and maintained osteoblastogenesis in vivo. Besides, miR-21-/- mice showed increased receptor activator of nuclear factor κB ligand (RANKL) and decreased osteoprotegerin (OPG) through miR-21 targeting Sprouty 1 (Spry1). Nevertheless, interestingly, miR-21 deficiency promoted trabecular bone mass accrual physiologically. Furthermore, in pathological states, the protection of bone mass was prominent in miR-21-/- mice. These skeletal effects were attributed to inhibition of bone resorption and osteoclast function by miR-21 deficiency through miR-21 targeting programmed cell death 4 (PDCD4), despite the existence of RANKL. As far as we know, this is the first in vivo evidence of a pro-osteoclastic microRNA. Together, these findings clarified function of miR-21 in bone metabolism, particularly uncovering osteo-protective potential of miR-21 inactivation in osteoporosis. 

Retracted: No

PubPeer comments:
 An image in Figure 6d appears to overlap with an image in Figure 7d, but they appear to be described differently. Apologies if I m misunderstanding something. *** ![file] *** This work was supported by grants from The National Natural Science Foundation of China (31301062 and 81271013). , 
 Dear Dr. Actinopolyspora biskrensis, Thank you for the careful reading of our published article. After checking all original data that underlie this study, we found that the image for Figure 7d, the u201cWT, agedu201d group, was wrongly used in figure assembly. We apologize for the mistake and will contact the editorial office for potential correction of the above paper. Best wishes, Yan Jin ,
Circular RNA hsa_circ_0000554 promotes progression and elevates radioresistance through the miR-485-5p/fermitin family members 1 axis in esophageal cancer
Authors: Jianhua Wang
Rui Wu
Yong Lin
Yushan Chen
Journal: Anti-Cancer Drugs (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Esophageal cancer; Circular RNA; FERMT1; Radioresistance; miR-485-5p
Affiliations: Department of Radiotherapy, Taizhou Hospital of Zhejiang Province, Taizhou, Zhejiang., Department of Radiology, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian., Department of Gastrointestinal Surgery, Houma People's Hospital, Linfen, Shanxi., Department of Cardiothoracic Surgery, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian, China.

Abstract:  Esophageal cancer is one of the most aggressive malignant cancers in the world. Circular RNA hsa_circ_0000554 (circ_0000554) and Fermitin family members 1 (FERMT1) are rated to the advancement of esophageal cancer. Nevertheless, the regulatory mechanisms between circ_0000554 and FERMT1 in the radioresistance of esophageal cancer are unclear. Quantitative real-time PCR (qRT-PCR) was applied to examine the expression of circ_0000554, FERMT1 mRNA, and miR-485-5p. Western blot analysis was employed to assess the protein expression levels of FERMT1, Ki-67, matrix metalloproteinase (MMP)-9 and MMP-2. Cell colony formation, migration, invasion, radiosensitivity and apoptosis were evaluated by cell colony formation, transwell or flow cytometry assays. The relationship between circ_0000554 or FERMT1 and miR-485-5p was verified with dual-luciferase reporter assay. Circ_0000554 and FERMT1 expression was enhanced in esophageal cancer tissues and radioresistant esophageal cancer tissues. Both circ_0000554 and FERMT1 repression blocked cell colony formation, migration, invasion and elevated cell radiosensitivity and apoptosis in esophageal cancer cells. Importantly, circ_0000554 served as a sponge for miR-485-5p in esophageal cancer cells. And FERMT1 acted as a downstream target for miR-485-5p. Additionally, circ_0000554 modulated FERMT1 expression via miR-485-5p. Furthermore, FERMT1 enhancement reversed circ_0000554 inhibition-mediated effects on the colony formation, migration, invasion, radiosensitivity and apoptosis of esophageal cancer cells. Circ_0000554 silencing repressed EC progression and enhanced cell radiosensitivity through downregulating FERMT1 via sponging miR-485-5p, which provided a possible method for improving the radioresistence of esophageal cancer. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A127 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern, and 2 have been retracted. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Effects of hepatocyte growth factor on phosphorylation of extracellular signal-regulated kinase and hippocampal cell death in rats with transient forebrain ischemia
Authors: Hiroshi Funakoshi
Makiko Niimura
Satoshi Takeo
Norio Takagi
Keiko Takagi
Toshikazu Nakamura
Journal: European Journal of Pharmacology (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Hepatocyte growth factor; neuronal cell death; hippocampal CA1 region; transient forebrain ischemia; intracellular signaling pathway
Affiliations: Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.

Abstract:  Hepatocyte growth factor (HGF) has been implicated in protection against several types of cell injuries. We investigated the effects of human recombinant HGF (hrHGF) on the selective neuronal cell death in the hippocampal CA1 region after transient forebrain ischemia in rats and explored the nature of the intracellular signaling pathway for the protection against this neuronal injury. hrHGF was injected continuously into the hippocampal CA1 region directly using an osmotic pump from 10 min to 72 h after the start of reperfusion. The marked increase in the number of TUNEL-positive cells found in the CA1 region after ischemia was almost completely abolished by the hrHGF treatment. Akt phosphorylation as well as IkappaB phosphorylation, which has been implicated in events downstream of the Akt, was not affected by hrHGF treatment. Extracellular signal-regulated kinase (ERK) phosphorylation was decreased in the CA1 region with time after ischemia. hrHGF increased or recovered ERK phosphorylation without changing the total amount of ERK protein. Immunohistochemical analysis demonstrated that phosphorylated ERK was colocalized with a neuronal nucleus marker NeuN in the hippocampal CA1 region of ischemic rats with hrHGF treatment at the early period after reperfusion. These results suggest that the protective effects of hrHGF against neuronal death in the hippocampal CA1 after transient forebrain ischemia could be related to an ERK-dependent pathway. 

Retracted: No

PubPeer comments:
 Total c-Met is identical in Figure 5B and D: ![file] In Figure 5C, c-Met is identical between 6 and 24hr: ![file] In Figure 6A, Akt bands in 1 and 24 hr are identical: ![file] In Figure 6C, 1 and 6 hours is identical, just flipped and the intensity is changed slightly: ![file] Figure 7, total ERK1 2 seems to be highly similar between 1 and 6 hr, just rotated slightly: ![file] ,