PReD-Bench/PRed-Bench huggingface dataset:
Elevated microRNA-129-5p level ameliorates neuroinflammation and blood-spinal cord barrier damage after ischemia-reperfusion by inhibiting HMGB1 and the TLR3-cytokine pathway
Authors: Hong Ma
Feng-Shou Chen
Wen-Fei Tan
Bo Fang
Xiao-Qian Li
Zai-Li Zhang
Journal: Journal of Neuroinflammation (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Blood-spinal cord barrier; High-mobility group box-1; Ischemia-reperfusion injury; MicroRNAs; Toll-like receptor 3.
Affiliations: Department of Anesthesiology, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China., Department of Anesthesiology, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China. .

Abstract:  Background: Ischemia-reperfusion (IR) affects microRNA (miR) expression and causes substantial inflammation. Multiple roles of the tumor suppressor miR-129-5p in cerebral IR have recently been reported, but its functions in the spinal cord are unclear. Here, we investigated the role of miR-129-5p after spinal cord IR, particularly in regulating high-mobility group box-1 (HMGB1) and the Toll-like receptor (TLR)-3 pathway. Methods: Ischemia was induced via 5-min occlusion of the aortic arch. The relationship between miR-129-5p and HMGB1 was elucidated via RT-PCR, western blotting, and luciferase assays. The cellular distribution of HMGB1 was determined via double immunofluorescence. The effect of miR-129-5p on the expression of HMGB1, TLR3, and downstream cytokines was evaluated using synthetic miRs, rHMGB1, and the TLR3 agonist Poly(I:C). Blood-spinal cord barrier (BSCB) permeability was examined by measuring Evans blue (EB) dye extravasation and the water content. Results: The temporal miR-129-5p and HMGB1 expression profiles and luciferase assay results indicated that miR-129-5p targeted HMGB1. Compared with the Sham group, the IR group had higher HMGB1 immunoreactivity, which was primarily distributed in neurons and microglia. Intrathecal injection of the miR-129-5p mimic significantly decreased the HMGB1, TLR3, interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels and the double-labeled cell count 48 h post-surgery, whereas rHMGB1 and Poly(I:C) reversed these effects. Injection of miR-129-5p mimic preserved motor function and prevented BSCB leakage based on increased Basso Mouse Scale scores and decreased EB extravasation and water content, whereas injection rHMGB1 and Poly(I:C) aggravated these injuries. Conclusions: Increasing miR-129-5p levels protect against IR by ameliorating inflammation-induced neuronal and BCSB damage by inhibiting HMGB1 and TLR3-associated cytokines. 

Retracted: No

PubPeer comments:
 Some images in figure 6a appear to overlap. Boxes show approximate area in the first column, however the adjacent photos appear to overlap in the same locations. Yellow box is approximate, as this image appears rotated 90u00b0. *** ![file] *** Full figure ![file] ,
Impact of surface coating and particle size on the uptake of small and ultrasmall superparamagnetic iron oxide nanoparticles by macrophages
Authors: Yoshichika Yoshioka
Shigeyoshi Saito
Yuki Mori
Daichi Koto
Kenya Murase
Mana Tsugeno
Satoshi Nohara
Journal: International Journal of Nanomedicine (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MRI; cultured mouse macrophage cells; particle size; surface coating; ultrasmall superparamagnetic iron oxide.
Affiliations: Department of Medical Physics and Engineering, Division of Medical Technology and Science, Faculty of Health Science, Graduate School of Medicine, Osaka University, Osaka, Japan.

Abstract:  Purpose: Magnetic resonance imaging (MRI) using contrast agents like superparamagnetic iron oxide (SPIO) is an extremely versatile technique to diagnose diseases and to monitor treatment. This study tested the relative importance of particle size and surface coating for the optimization of MRI contrast and labeling efficiency of macrophages migrating to remote inflammation sites. Materials and methods: We tested four SPIO and ultrasmall superparamagnetic iron oxide (USPIO), alkali-treated dextran magnetite (ATDM) with particle sizes of 28 and 74 nm, and carboxymethyl dextran magnetite (CMDM) with particle sizes of 28 and 72 nm. Mouse macrophage RAW264 cells were incubated with SPIOs and USPIOs, and the labeling efficiency of the cells was determined by the percentage of Berlin blue-stained cells and by measuring T(2) relaxation times with 11.7-T MRI. We used trypan blue staining to measure cell viability. Results: Analysis of the properties of the nanoparticles revealed that ATDM-coated 74 nm particles have a lower T(2) relaxation time than the others, translating into a higher ability of MRI negative contrast agent. Among the other three candidates, CMDM-coated particles showed the highest T(2) relaxation time once internalized by macrophages. Regarding labeling efficiency, ATDM coating resulted in a cellular uptake higher than CMDM coating, independent of nanoparticle size. None of these particle formulations affected macrophage viability. Conclusion: This study suggests that coating is more critical than size to optimize the SPIO labeling of macrophages. Among the formulations tested in this study, the best MRI contrast and labeling efficiency are expected with ATDM-coated 74 nm nanoparticles. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
One-Year Freedom from Amputation, Survival, and Cost of Care following Tibial and Pedal Endovascular Interventions for Critical Limb Ischemia: The Role of Atherectomy and Drug-Eluting Stents
Authors: Fred Rahimi
Sapan S Desai
Neal Shukla
Hyim Baronofsky
Journal: Annals of Vascular Surgery (2020)
Discipline: CLINICAL MEDICINE
Keywords: Article withdrawal; Author(s); Editor; Publisher; Elsevier Policy
Affiliations: Northwest Community Healthcare, Arlington Heights, IL. Electronic address: ., Northwest Community Healthcare, Arlington Heights, IL., First Step Foot Care, Arlington Heights, IL.

Abstract:  This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal 

Retracted: No

PubPeer comments:
 Figure 4B. * Aqua arrows: three panels displaying different biosensors and proteins appear to show five lanes in common, albeit in different orientations * Red arrows: two panels displaying different biosensors and proteins appear to show four lanes in common, albeit in different orientations ![file] Reported to the journal in October 2015. , 
 Figure 6A. * Pink arrows: three panels displaying different proteins appear to have 4 lanes in common, albeit in there different orientations. ![file] ,
MicroRNA-203 inhibits malignant melanoma cell migration by targeting versican
Authors: Pingyuan Bu
Ping Yang
Journal: Experimental and therapeutic medicine (2014)
Discipline: CLINICAL MEDICINE
Keywords: malignant melanoma; microRNA-203; migration; versican.
Affiliations: Department of Burns, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.

Abstract:  MicroRNA (miR)-203 has been demonstrated to function as a suppressor in tumorigenesis. Recently, miR-203 was reported to play a role in malignant melanoma (MM); however, the detailed function of miR-203 in MM remains unclear. In the present study, the expression of miR-203 was shown to be significantly downregulated in MM tissues when compared with normal adjacent tissues. Based on a bioinformatic prediction, versican was further identified as a novel target of miR-203, and the expression of versican was markedly increased in MM tissues. Inhibition of miR-203 increased the protein expression of versican, while upregulation of miR-203 inhibited the protein expression of versican in MM A375 cells. In addition, the upregulation of versican significantly promoted A375 cell migration; however, upregulation of miR-203 suppressed A375 cell migration. The present study further investigated whether miR-203 was involved in versican-mediated A375 cell migration, and the results indicated that upregulation of miR-203 significantly inhibited A375 cell migration, which was impaired by overexpression of versican. These observations indicated that versican functions as a downstream effector in miR-203-mediated MM cell migration. Therefore, the results demonstrated that miR-203 exhibited an inhibitory effect on MM cell migration via directly targeting versican, thus, may become an effective inhibitor for MM metastasis. 

Retracted: No

PubPeer comments:
 Irrelevant citation. ![file] ![file] , 
 The value max_E of row E1 in Table 2 for LSTM does not match that in Fig. 3. ![file] ![file] ![file] , 
 The curve  Daily average load curve in Fig. 3 is not explained and looks confusing compared to  actual load curve . ,
Effects of fibroblast growth factors 2 and low intensity pulsed ultrasound on the repair of knee articular cartilage in rabbits
Authors: Z-F Tang
H-Y Li
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: low intensity ultrasound; fibroblast growth factors (FGF2); knee articular cartilage repair; rabbit; histopathological changes
Affiliations: Department of Orthopedics, Yantaishan Hospital, Yantai, China. .

Abstract:  Objective: To investigate the effect of low intensity ultrasound irradiation combine with fibroblast growth factors (FGF2) on the repair of the knee articular cartilage and to explore its mechanism in rabbit. Materials and methods: The model of the rabbit knee joint injury was established. 40 rabbits were divided into four groups, including control group, model group, FGF2 group and FGF2 + low intensity pulsed ultrasound group (FGF2 + LIPU). The knee joints of rabbits were taken at 4 and 8 weeks, respectively. Histopathological changes were detected by Hematoxylin and Eosin stain (HE) and evaluated by Wakitani score. The expression of FGF2 mRNA was detected by Real-time polymerase chain reaction (RT-PCR) and the levels of Collagen I and Collagen II protein were analyzed by Western blotting. Results: In FGF2 group and FGF2 + LIPU group, it was found that the tissues of knee joint were gradually repaired following the change of time. Further, the recovery was better in FGF2 + LIPU group. Cartilage defect areas were filled with cartilage-like cells and the repair surface was fused with surrounding cartilage in FGF2 and FGF2 + LIPU groups. Wakitani scores were consistent with HE results. The expressions of FGF2 mRNA were higher in FGF2 and FGF2 + LIPU group than the model group. Western blotting results showed that the levels of Collagen I and Collagen II protein in FGF2 and FGF2 + LIPU groups were significantly increased compared with that in model group. Conclusions: FGF2 and LIPU combined application on the rabbit knees joint repair is better than FGF2 alone. FGF2 and LIPU combination can promote the synthesis and secretion of collagen in chondrocytes, promote the differentiation and maturation of chondrocytes during the repair of cartilage defects. 

Retracted: No

PubPeer comments:
 Here is the link to the 2014 u201c**[Corrigendum] ** on Pub Peer: https: pubpeer.com publications D69DE2E1620A86BE30004C0E458326 Here is the link to the u201c**[Corrigendum] **u201d on the Oxford University Press web site: https: academic.oup.com jcem article 99 12 4758 2834758 Corrigendum, The Journal of Clinical Endocrinology Metabolism, Volume 99, Issue 12, December 2014, Pages 4758u20134759, https: doi.org 10.1210 jc.2014-3926 ,
<i>Retracted</i> : Silencing of keratin 1 inactivates the Notch signaling pathway to inhibit renal interstitial fibrosis and glomerular sclerosis in uremia
Authors: Li-Na Sun
Zhong-Qi Zhou
Yu-Lin Man
Wen Chen
Yue-Qin Ren
Lei Zhang
Zhi-Kui Wang
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: glomerular sclerosis; keratin 1; kidney interstitial fibrosis; notch pathway; uremia.
Affiliations: Department of Nephrology Linyi People's Hospital  Linyi China

Abstract:  Renal interstitial fibrosis is a key factor in the development of chronic renal diseases, possibly leading to uremia. The present study conducted aimed to assess the hypothesis whether keratin 1 (KRT1) silencing could suppress kidney interstitial fibrosis and glomerular sclerosis via the Notch pathway to alleviate uremic symptoms. Differentially expressed genes associated with uremia were identified using the gene expression omnibus (GEO) database. Uremic rat models were established, in which short hairpin-RNA against KRT1, activators, and inhibitors of the Notch pathway were transfected. To further validate the mechanism of KRT1 in uremia, KRT1 expression, cell apoptosis, glomerular area (GA), and glomerular capillary volume (GV), the score of glomerular sclerosis, and tubulointerstitial injury were assayed and investigated. GEO database revealed that KRT1 was upregulated in uremia and regulated the Notch pathway. GA, GV, cell apoptosis, glomerular sclerosis, and tubulointerstitial injury were typically located in more elevated levels of uremia in rats. KRT1 silencing and Notch pathway inhibition decreased the expression of Jagged1, Notch1, NICD1, Hey1, Hes1, α-SMA, and FN, which further resulted in decreased cell apoptosis, GA, GV, the score of glomerular sclerosis, and tubulointerstitial injury. Subsequently, the effect of KRT1 silencing on uremia was no longer evident once the Notch pathway was activated. The co-localization of high expression KRT1 and Notch1 was found in uremia. In summary, the results identified KRT1 as a key regulator in uremia progression, and KRT1 silencing can suppress glomerular sclerosis and tubulointerstitial injury via inactivation of the Notch pathway in uremic rats. 

Retracted: Yes

PubPeer comments:
 Retracted [8 March 2022] . ------------------------- The above article, published online on 20 August 2019 in Wiley Online Library , has been retracted by agreement between the authors, the journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed after the authors stated that unintentional errors occurred during the research process, and the experimental results cannot be verified. Thus, the conclusions are considered to be invalid. ,
Aceclofenac-loaded chondroitin sulfate conjugated SLNs for effective management of osteoarthritis
Authors: Ankit Jain
Sanjay K Jain
Pooja Hurkat
Mamta Bishnoi
Journal: Journal of Drug Targeting (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Joint; NSAIDs; osteophytes; pain.
Affiliations: Department of Pharmaceutical Sciences, Pharmaceutics Research Projects Laboratory, Dr. Hari Singh Gour Central University , Sagar, MP , India.

Abstract:  Abstract Background: In intra-articular drug delivery, there are number of shortcomings such as lymphatic drainage from the synovial cavity, frequent dosing, adverse side effects and patient discomfort in the management of osteoarthritis (OA). Purpose: This research work reports the development and characterization of aceclofenac-loaded chondroitin sulfate (CS) conjugated (CS-SLN) and unconjugated solid lipid nanoparticles (SLN) for the effective management of OA. Methods: The SLNs were prepared using modified solvent injection method and coupled with CS. They were further characterized for size and size distribution, zeta potential, surface morphology, % entrapment efficiency and in vitro drug release profile. Anti-inflammatory activity and in vivo performance was also predicted. Results: The particle size of the SLN and CS-SLN was found to be 143.4 ± 0.9 nm and 154.2 ± 1.1 nm, respectively. SLNs exhibited sustained drug release (SLN, 64.25 ± 0.75%; CS-SLN, 57.82 ± 0.62%) in vitro for more than 24 h. In vivo performance studies revealed the highest uptake of SLNs by the knee joint. Discussion: SLNs enhanced accumulation at the knee joint due to specific interactions with CD44, annexin and leptin receptors attributed to CS coupling. Conclusion: CS-SLN could be potentially effective vector for the treatment or management of OA. 

Retracted: No

PubPeer comments:
 Same image used after background alteration and rotation. ![file] ,
The ATM/ATR signaling effector Chk2 is targeted by Epstein-Barr virus nuclear antigen 3C to release the G2/M cell cycle block
Authors: Subhash C Verma
Ke Lan
Masanao Murakami
Erle S Robertson
Tathagata Choudhuri
Journal: Journal of Virology (2007)
Discipline: MICROBIOLOGY
Keywords: Epstein-Barr virus; EBV; B lymphocytes; EBNA3C; cell cycle checkpoint
Affiliations: Department of Microbiology and the Tumor Virology Program, Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, 201E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA., Department of Microbiology and The Tumor Virology Program of the Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Abstract:  Epstein-Barr virus (EBV) infects most of the human population and persists in B lymphocytes for the lifetime of the host. The establishment of latent infection by EBV requires the expression of a unique repertoire of genes. The product of one of these viral genes, the EBV nuclear antigen 3C (EBNA3C), is essential for the growth transformation of primary B lymphocytes in vitro and can regulate the transcription of a number of viral and cellular genes important for the immortalization process. This study demonstrates an associated function of EBNA3C which involves the disruption of the G2/M cell cycle checkpoint. We show that EBNA3C-expressing lymphoblastoid cell lines treated with the drug nocodazole, which is known to block cells at the G2/M transition, did not show a G2/M-specific checkpoint arrest. Analyses of the cell cycles of cells expressing EBNA3C demonstrated that the expression of this essential EBV nuclear antigen is capable of releasing the G2/M checkpoint arrest induced by nocodazole. This G2/M arrest in response to nocodazole was also abolished by caffeine, suggesting an involvement of the ATM/ATR signaling pathway in the regulation of this cell cycle checkpoint. Importantly, we show that the direct interaction of EBNA3C with Chk2, the ATM/ATR signaling effector, is responsible for the release of this nocodazole-induced G2/M arrest and that this interaction leads to the serine 216 phosphorylation of Cdc25c, which is sequestered in the cytoplasm by 14-3-3. Overall, our data suggest that EBNA3C can directly regulate the G2/M component of the host cell cycle machinery, allowing for the release of the checkpoint block. 

Retracted: No

PubPeer comments:
 Figure 2E. Some parts of the flow cytometry look similar to parts in other panels. Boxes of the same color draw attention to areas that look similar. ![file] Figure 4I appears to have the same problems, which I will leave for somebody else to color code. ,
MicroRNA-424 is down-regulated in hepatocellular carcinoma and suppresses cell migration and invasion through c-Myb
Authors: Lei Yu
YanFang Jiang
Changzhi He
Guo-feng Ding
Lei Sun
Liying Zhu
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Hepatocellular carcinoma; MicroRNAs; miR-424; Tumorigenesis; c-Myb
Affiliations: Department of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang, China., Department of Infectious Disease, Binzhou Medical University Hospital, Binzhou, Shandong, China., The Graduate School of Harbin Medical University, Harbin, Heilongjiang, China., Department of Ophthalmology, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang, China., Key Laboratory of Zoonosis Research, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun, Jilin, China; Department of Central Laboratory, the Second Part of First Hospital, Jilin University, Changchun, Jilin, China.

Abstract:  Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. MicroRNAs (miRNAs) are important regulators of multiple cellular processes, and the aberrant miRNAs expressions have been observed in different types of cancer including HCC. Their pathysiologic role and their relevance to tumorigenesis are still largely unknown. In this study, we demonstrated the down-regulation of miR-424 in HCC cell lines and tissues by quantitative RT-PCR analyses. Overexpression of miR-424 reduced the HCC cell prolifetation, migration, and invasion. Conversely, inhibiton of miR-424 expression significantly accelerated the cell proliferation, migration, and invasion. In addition, we further identified c-Myb as a functional downstream target of miR-424 by directly targeting the 3'UTR of c-Myb. Furthermore, overexpression of c-Myb impaired miR-424-induced inhibition of proliferation and invasion in HCC cells. Our results demonstrated that miR-424 was involved in tumorigenesis of HCC at least in part by suppression of c-Myb. 

Retracted: No

PubPeer comments:
null, 
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 2021 correction. https: journals.plos.org plosone article?id=10.1371 journal.pone.0252252 Following the publication of this article [1] concerns were raised regarding similarities between the ey-GAL4 results presented in Fig 2D and 2E. Similarly, concerns were raised regarding similarities between the GMR-GAL4 results presented in S3E and S3F Fig. The corresponding author explained that for each pair of figure panels (Fig 2D and 2E; S3E and S3F Fig) the results were obtained in the same blot experiment. Lanes from the same original blot image were spliced together to present pertinent results in each panel; the control data were reused in Fig 2D and 2E and in S3E and S3F Fig. Reference 1.Chang Y-J, Zhou L, Binari R, Manoukian A, Mak T, McNeill H, et al. (2016) The Rho Guanine Nucleotide Exchange Factor DRhoGEF2 Is a Genetic Modifier of the PI3K Pathway in Drosophila. PLoS ONE 11(3): e0152259. pmid:27015411 ,
Neuroprotective action of agmatine in rotenone-induced model of Parkinson’s disease: Role of BDNF/cREB and ERK pathway
Authors: Caner Günaydin
M Emin Önger
S Sırrı Bilge
Ayhan Bozkurt
Bahattin Avci
Journal: Behavioural Brain Research (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Agmatine; BDNF; ERK1/2; Rat; Rotenone
Affiliations: Ondokuz Mayıs University, School of Medicine, Department of Pharmacology, Samsun, Turkey. Electronic address: ., Ondokuz Mayıs University, School of Medicine, Department of Histology and Embryology, Samsun, Turkey. Electronic address: ., Ondokuz Mayıs University, School of Medicine, Department of Physiology, Samsun, Turkey. Electronic address: ., Ondokuz Mayıs University, School of Medicine, Department of Biochemistry, Samsun, Turkey. Electronic address: .

Abstract:  Numerous studies have investigated the role of agmatine in the central nervous system and indicated neuroprotective properties. In addition to its potent antioxidant effects, agmatine is an endogenous neuromodulator and has wide spectrum molecular actions on different receptor subtypes (NMDA, Imidazoline 1-2, alpha-2 adrenoreceptor, 5-HT2a, 5-HT3) and cellular signaling pathways (MAPK, PKA, NO, BDNF). Although the neuroprotective effects of agmatine demonstrated in experimental Parkinson's disease model, the effects of agmatine with the aspect of neuroplasticity and possible signaling mechanisms behind agmatine actions have not been investigated. Herein, in this study, we investigated the role of the of agmatine on rotenone-induced Parkinson's disease model. Agmatine at the dose of 100 mg/kg i.p., was mitigated oxidative damage and alleviated motor impairments which were the results of the rotenone insult. Additionally, agmatine decreased neuronal loss, tyrosine hydroxylase immunoreactivity and increased cREB, BDNF and ERK1/2 expression in the striatum, which are crucial neuroplasticity elements of striatal integrity. Taken together, the present study expands the knowledge of molecular mechanisms behind neuroprotective actions of agmatine in Parkinson's disease, and as far as we have known, this is the first study to delineate agmatine treated activation of cellular pathways which are important elements in neuronal cell survival. 

Retracted: No

PubPeer comments:
 Image duplication in Fig 8. ![file] Image duplication in Fig 6 with  Neuroscience Letters 699 (2019) 71-76 ![file] ,
Anti-Invasion and Antimetastatic Effects of Porcine Recombinant NK-lysin on SMMC-7721 Human Hepatocellular Carcinoma Cells
Authors: Kuohai Fan
Zhirui Wang
Hongquan Li
Wenjuan Du
Ajab Khan
Junbing Jiang
Journal: BioMed Research International (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: hepatocellular carcinoma; invasion; metastasis; NK-lysin; SMMC-7721 cells
Affiliations: Laboratory Animal Center, Shanxi Agricultural University, Taigu, Shanxi, China, College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, China, Plastic & Reconstructive Surgery, University of Colorado Denver, Denver, CO, USA

Abstract:  The high invasion and metastasizing abilities of hepatocellular carcinoma (HCC) are the primary reasons for the high mortality rate of patients. Therefore, identification of agents to inhibit invasion and metastasis is very important for treatment of HCC. We analyzed the anti-invasion and antimetastatic effects of porcine recombinant NK-lysin, which was designed and expressed in vitro by our research group, on SMMC-7721 hepatocellular carcinoma cells via wound-healing assays, adhesion assays, invasion assays, real-time polymerase chain reaction (PCR), and Western blot analysis. MTT assay results indicated that NK-lysin inhibited the growth of SMMC-7721 cells in a dose- and time-dependent manner. NK-lysin reduced the ability of cell migration, adhesion, and invasion. Based on gene and protein expression analysis, NK-lysin decreased β-catenin and MMP-2 expression. These results suggested that NK-lysin has anti-invasion and antimetastatic effects on hepatocellular carcinoma cells in vitro by reducing the level of the β-catenin and MMP-2. 

Retracted: No

PubPeer comments:
 ![file] ,
Phosphorylation of IkappaB-beta is necessary for neuronal survival
Authors: Santosh R D&#x27;Mello
Li Liu
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cerebellar granule neurons; apoptosis; potassium; IkappaB-beta; phosphorylation
Affiliations: Department of Molecular and Cell Biology, University of Texas, Richardson, Texas 75083, USA.

Abstract:  Cerebellar granule neurons undergo apoptosis when switched from culture medium containing depolarizing levels of potassium (high potassium or HK) to nondepolarizing medium (low potassium or LK). We showed that in healthy neurons maintained in HK medium, IkappaB-beta is phosphorylated at a novel site, Tyr-161. LK-induced neuronal apoptosis is accompanied by a decrease in the extent of IkappaB-beta phosphorylation at this residue. Tyr-161 shares similarity to the consensus sequence for phosphorylation by the nonreceptor tyrosine kinases Abl and Arg. Arg phosphorylates Tyr-161 differentially in vitro, and LK treatment does cause a down-regulation of Arg activity. Moreover, treatment of neurons with two structurally distinct and highly selective Abl inhibitors, PD173955 and Gleevec, blocks HK-induced phosphorylation of IkappaB-beta at Tyr-161 and induces neuronal apoptosis. Overexpression of wild-type IkappaB-beta blocks LK-induced apoptosis, but this effect is abolished when Arg is pharmacologically inhibited. On the other hand, forced overexpression of IkappaB-beta in which Tyr-161 is mutated inhibits survival in HK demonstrating the importance of this residue to neuronal survival. Phosphorylation of IkappaB-beta enhances its association with p65/RelA causing an increase in NF-kappaB DNA binding activity. Our results identified IkappaB-beta phosphorylation as a key event in neuronal survival and provided a mechanism by which this is mediated. 

Retracted: No

PubPeer comments:
 Figure 4A. https: imgur.com S5kz8uR ,
LncRNA lncLy6C induced by microbiota metabolite butyrate promotes differentiation of Ly6Chigh to Ly6Cint/neg macrophages through lncLy6C/C/EBPβ/Nr4A1 axis
Authors: Rongcun Yang
Houbao Qi
Jiang Zhou
Jianmei Yue
Xinqi Liu
Yuan Zhang
Jianmei Wei
Yazheng Yang
Yunhuan Gao
Journal: Cell Discovery (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Macrophages; differentiation; transcription factors; lncLy6C; gut microbiota metabolites
Affiliations: Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin 300071, China., State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China., Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin 300071, China., College of life Science, Nankai University, Tianjin 300071, China., Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin 300071, China. ., State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China. ., Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin 300071, China. .

Abstract:  Macrophages are mainly divided into two populations, which play a different role in physiological and pathological conditions. The differentiation of these cells may be regulated by transcription factors. However, it is unclear how to modulate these transcription factors to affect differentiation of these cells. Here, we found that lncLy6C, a novel ultraconserved lncRNA, promotes differentiation of Ly6Chigh inflammatory monocytes into Ly6Clow/neg resident macrophages. We demonstrate that gut microbiota metabolites butyrate upregulates the expression of lncLy6C. LncLy6C deficient mice had markedly increased Ly6Chigh pro-inflammatory monocytes and reduced Ly6Cneg resident macrophages. LncLy6C not only bound with transcription factor C/EBPβ but also bound with multiple lysine methyltransferases of H3K4me3 to specifically promote the enrichment of C/EBPβ and H3K4me3 marks on the promoter region of Nr4A1, which can promote Ly6Chigh into Ly6Cneg macrophages. As a result, lncLy6C causes the upregulation of Nr4A1 to promote Ly6Chigh inflammatory monocytes to differentiate into Ly6Cint/neg resident macrophages. 

Retracted: No

PubPeer comments:
 Is this a typical way of using this staining method? Fig 2 - H ![file] , 
 This figure need to wait for a while, This student has other things. He come back, we will reply to you ,
Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells
Authors: Julieta M Ceruti
Cecilia L Varone
María E Scassa
Juan M Fló
Eduardo T Cánepa
Journal: Oncogene (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: genetic instability; tumorigenesis; DNA damage; DNA replication; integrated response
Affiliations: Laboratorio de Biología Molecular, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria Pabellón II Piso 4, 1428 Buenos Aires, Argentina.

Abstract:  The genetic instability driving tumorigenesis is fueled by DNA damage and by errors made by the DNA replication. Upon DNA damage the cell organizes an integrated response not only by the classical DNA repair mechanisms but also involving mechanisms of replication, transcription, chromatin structure dynamics, cell cycle progression, and apoptosis. In the present study, we investigated the role of p19INK4d in the response driven by neuroblastoma cells against DNA injury caused by UV irradiation. We show that p19INK4d is the only INK4 protein whose expression is induced by UV light in neuroblastoma cells. Furthermore, p19INK4d translocation from cytoplasm to nucleus is observed after UV irradiation. Ectopic expression of p19INK4d clearly reduces the UV-induced apoptosis as well as enhances the cellular ability to repair the damaged DNA. It is clearly shown that DNA repair is the main target of p19INK4d effect and that diminished apoptosis is a downstream event. Importantly, experiments performed with CDK4 mutants suggest that these p19INK4d effects would be independent of its role as a cell cycle checkpoint gene. The results presented herein uncover a new role of p19INK4d as regulator of DNA-damage-induced apoptosis and suggest that it protects cells from undergoing apoptosis by allowing a more efficient DNA repair. We propose that, in addition to its role as cell cycle inhibitor, p19INK4d is involved in maintenance of DNA integrity and, therefore, would contribute to cancer prevention. 

Retracted: No

PubPeer comments:
 Figure 2b. Much more similar than expected. https: imgur.com eeJI5bp ,
Long non-coding RNA MACC1-AS1 promoted pancreatic carcinoma progression through activation of PAX8/NOTCH1 signaling pathway
Authors: Chen Qi
Li Dongen
Chen Xiaofeng
Xu Liping
Jiang Jianshuai
Hu Yue
Yang Liang
Journal: Journal of Experimental & Clinical Cancer Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: Long ncRNAs (lncRNAs); Metastasis; Pancreatic carcinoma (PC); Proliferation; Pyruvate kinase M2 (PAX8).
Affiliations: Department of Hepatobiliary & Pancreatic Surgery, Ningbo First Hospital, No. 59 Liuting Street, Haishu District, Ningbo, 315000, Zhejiang Province, China., Department of Hepatobiliary & Pancreatic Surgery, Ningbo First Hospital, No. 59 Liuting Street, Haishu District, Ningbo, 315000, Zhejiang Province, China. .

Abstract:  Background: Accumulated evidences have demonstrated that long non-coding RNAs (lncRNAs) are dysregulated and correlate with the pathophysiological basis of malignant tumors. The objective of this research is to uncover the possible molecular mechanism of MACC1-AS1 regarding the regulation of pancreatic carcinoma (PC) metastasis. Methods: lncRNA microarray and qRT-PCR were applied to identify differentially expressed lncRNA profile in PC. The function and role of MACC1-AS1 in PC were assessed via in vitro as well as in vivo assays. Luciferase analyses, RNA immunoprecipitation, and RNA pull-down were performed to determined the underlying MACC1-AS1 mechanisms. Results: Numbers of differentially expressed lncRNAs in PC were identified via lncRNA microarrays, among which MACC1-AS1 was revealed as the most abundant lncRNA. The upregulation of MACC1-AS1 in PC was further confirmed in two expanded PC cohorts, which showed that MACC1-AS1 expression was upregulated in those PC patients with poor survival. Functionally, knockdown of MACC1-AS1 inhibited the proliferation as well as metastasis of PC cells. Meanwhile, MACC1-AS1 upregulated the expression of PAX8 protein, which promoted aerobic glycolysis and activated NOTCH1 signaling. Additionally, PAX8 was upregulated in PC tissues, which was correlated with the expression of MACC1-AS1 and the overall survival of PC patients. Conclusions: Together, our findings indicate a critical role of MACC1-AS1/PAX8/NOTCH1 signaling, which may be an alternative treatment target in PC therapy. 

Retracted: No

PubPeer comments:
 At least one image in Figure 5A appears to have some internal features which repeat, or nearly repeat (orange, yellow). *** ![file] *** ![file] , 
 At least two images in Figure 2F appear to have similar issues. *** ![file] *** Showing location ![file] , 
 Another overlap in 2F with a change in dimensions and color. H T Dr. Bik *** ![file] ,
Disturbances of diurnal phase markers, behavior, and clock genes in a rat model of depression; modulatory effects of agomelatine treatment
Authors: K Højgaard
E V Bouzinova
O Wiborg
S L Christiansen
Journal: Psychopharmacology (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Agomelatine; Chronic mild stress model; Clock gene expression; Depression; Melatonin.
Affiliations: Department of Clinical Medicine, Aarhus University, Aarhus, Denmark., Center of Functionally Integrative Neuroscience, Department of Clinical Medicine, Health, Aarhus University, Nørrebrogade 44, Building 10G, 8000, Aarhus C, Denmark. .

Abstract:  Major depressive disorder (MDD) is a growing problem worldwide. Though, the etiology remains unresolved, circadian rhythm disturbances are frequently observed in MDD and thus is speculated to play a key role herein. The present study focuses on circadian rhythm disturbances in the chronic mild stress (CMS) animal model of depression and examined whether the atypical antidepressant, agomelatine, which is mediating its action via melatonergic and serotonergic receptors, is capable of resynchronizing the perturbed rhythm. Melatonin is often used as a marker of the circadian phase, but the functional and behavioral output is dictated on a cellular level by the molecular clock, driven by the clock genes. We applied in situ hybridization histochemistry to measure the expression levels of the core clock genes, period (Per) 1 and 2 and bone and muscle ARNT-like protein 1 (Bmal1), in multiple brain regions believed to be implicated in depression. Agomelatine showed an antidepressant-like effect in the sucrose consumption test and an anxiolytic-like profile in the elevated zero maze. We found that CMS increased nighttime melatonin release in rats and that agomelatine attenuated this effect. Stress was shown to have a time and region-specific effect on clock gene expression in the brain. Treatment with agomelatine failed to normalize clock gene expression, and the observed modifying effect on gene expression did not associate with the antidepressant-like effect. This suggests that the antidepressant actions of agomelatine are mainly independent of circadian rhythm synchronization and, in this regard, not superior to traditional antidepressants tested in our model. 

Retracted: No

PubPeer comments:
 Figure 6. * Four panels appear to look similar to each other, albeit in mirrored orientation. Reported to the journal in October 2015, but nothing has been done as of today. ![file] ,
Impact of Early Cannulation Grafts on Quality and Cost of Care for Patients With End-Stage Renal Disease
Authors: Sapan S Desai
Journal: Annals of Vascular Surgery (2019)
Discipline: CLINICAL MEDICINE
Keywords: End-stage renal disease (ESRD); hemodialysis; cannulation arteriovenous grafts (ECAVGs); central venous catheters (CVCs); cost of care
Affiliations: Director of Performance Improvement, Northwest Community Healthcare, Arlington Heights, IL. Electronic address: .

Abstract:  Background: The annual cost of care associated with end-stage renal disease (ESRD) per patient on hemodialysis is approaching $100,000, with nearly $42 billion in national spend per year. Early cannulation arteriovenous grafts (ECAVGs) help decrease the use of central venous catheters (CVCs), thus potentially decreasing the cost of care. However, a formal financial analysis that also includes the cost of CVC-related complications and secondary interventions has not been completed. The purpose of this project is to evaluate the overall financial costs associated with ECAVGs on patients with ESRD during a one-year period. Methods: Access modality, complications, secondary interventions, hospital outcomes, and cost of care were determined for 397 sequential patients who underwent access creation between July 2014 and October 2018. A detailed financial analysis was completed, including an evaluation of implant, supplies, medications, laboratories, labor, and other direct costs. All variables were measured at the time of the index procedure, 30 days, 90 days, 180 days, 270 days, and one year. Results: There were 131 patients who underwent arteriovenous fistula (AVF) and 266 who underwent ECAVG for dialysis access. The average cost of care was $17,523 for AVF and $5,894 for ECAVG at one year (P &lt; 0.01). Fewer CVC-related complications and secondary interventions associated with ECAVGs saved $11,630 per patient with ESRD, primarily in the form of supply costs. Fewer CVCs in the patients receiving ECAVGs led to an additional $1,083 decrease in cost associated with sepsis reduction at one year. A subsequent decrease in length of stay and ICU utilization led to an additional $2.0 million decrease in annual cost of care for patients with ESRD. Conclusions: The use of ECAVGs has significant cost savings over using an AVF and CVC for urgent-start dialysis in patients with ESRD. This cost savings is secondary to decreased CVC-related complications and fewer secondary interventions. Significant national savings are possible with appropriate use of ECAVGs in patients with ESRD. 

Retracted: No

PubPeer comments:
 This paper does not have a conflict of interest statement, which is unusual for a medical journal. ,
Atherogenic lipids induce adhesion of human coronary artery smooth muscle cells to macrophages by up-regulating chemokine CX3CL1 on smooth muscle cells in a TNFalpha-NFkappaB-dependent manner
Authors: Yuan Zhang
Philip M Murphy
Jana Barlic
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: genetic evidence; adhesive chemokine; CX3CL1; leukocyte receptor; CX3CR1

Abstract:  Recent genetic evidence has implicated the adhesive chemokine CX3CL1 and its leukocyte receptor CX3CR1 in atherosclerosis. We previously proposed a mechanism involving foam cell anchorage to vascular smooth muscle cells because: 1) CX3CL1 and CX3CR1 are expressed by both cell types in mouse and human atherosclerotic lesions; 2) foam cells are reduced in lesions in cx3cr1(-/-)apoE(-/-) mice; and 3) proatherogenic lipids (oxidized low density lipoprotein [oxLDL] and oxidized linoleic acid derivatives) induce adhesion of primary human macrophages to primary human coronary artery smooth muscle cells (CASMCs) in vitro in a macrophage CX3CR1-dependent manner. Here we analyze this concept further by testing whether atherogenic lipids regulate expression and function of CX3CL1 and CX3CR1 on CASMCs. We found that both oxLDL and oxidized linoleic acid derivatives indirectly up-regulated CASMC CX3CL1 at both the protein and mRNA levels through an autocrine feedback loop involving tumor necrosis factor alpha production and NF-kappaB signaling. Oxidized lipids also up-regulated CASMC CX3CR1 but through a different mechanism. Oxidized lipid stimulation also increased adhesion of macrophages to CASMCs when CASMCs were stimulated prior to assay, and a synergistic pro-adhesive effect was observed when both cell types were prestimulated. Selective inhibition with a CX3CL1-specific blocking antibody indicated that adhesion was strongly CASMC CX3CL1-dependent. These findings support the hypothesis that CX3CR1 and CX3CL1 mediate heterotypic anchorage of foam cells to CASMCs in the context of atherosclerosis and suggest that this chemokine/chemokine receptor pair may be considered as a pro-inflammatory target for therapeutic intervention in atherosclerotic cardiovascular disease. 

Retracted: No

PubPeer comments:
 The flow cytometry dot plots in blue boxes appear to look similar in Fig 1A. The percentages of cells are different. ![file] ,
LncRNA BX357664 inhibits the proliferation and invasion of non-small cell lung cancer cells
Authors: B Li
Y-M Du
J Yang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; BX357664; NSCLC; tumor staging; lymph node metastasis
Affiliations: Department of Pathology, Jinzhou Medical University, Jinzhou, China. .

Abstract:  Objective: To explore the level of long non-coding RNA (lncRNA) BX357664 in non-small cell lung cancer (NSCLC) and its role in the development of NSCLC. Meanwhile, the potential regulatory mechanism of BX357664 was also what we were interested in. Patients and methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to examine the level of BX357664 in 82 pairs of cancer tissues and adjacent normal tissues collected from patients with NSCLC, and the relationship between BX357664 level and pathological parameters or prognosis of NSCLC patients was analyzed. Further verification by RT-qPCR was to examine BX357664 expression in NSCLC cell lines, and BX357664 overexpression model was constructed using lentivirus in NSCLC cell lines including SPCA1 and H1299. In addition, cell counting kit-8 (CCK-8), cell clone formation assay, and transwell assay were performed to analyze the influence of BX357664 on the biological function of NSCLC cells. Western Blot was conducted to explore its underlying mechanisms. Results: RT-qPCR results indicated that BX357664 in NSCLC was remarkably lower than that in normal tissues. Compared with patients with highly-expressed BX357664, patients with lowly-expressed had worse tumor stage, higher incidence of lymph node metastasis or distant metastasis and lower overall survival rate. In addition, compared with NC group, the proliferation, invasion and migration ability of cells in BX357664 overexpression group was attenuated significantly, and the key proteins in TGF-β1/Smad pathway including transforming growth factor-β1 (TGF-β1), p-Smad2, p-Smad3, N-cad, Vimentin and MMP-9 were also remarkably reduced. Conclusions: BX357664 level was significantly reduced in tumor tissues of NSCLC patients, resulting in advanced tumor staging, lymph node metastasis, distant metastasis, and poor prognosis. Additionally, BX357664 may inhibit the proliferation as well as invasion and migration of NSCLC cells by regulating TGF-β1/Smad pathway. 

Retracted: Yes

PubPeer comments:
  This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. As is the custom of this journal, readers are left to speculate on the reason for retraction. I ll begin by pointing out that the paper appears to be from the  Comb papermill . Products of that studio are marked by (among other features) - a Table 1 in which the column headings promise to convert numbers in each patient subgroup into percentages, without delivering; and - pairs of Kaplan-Meier survival plots, crenellated along the top so as to resemble combs or walls built of Lego, where survival nose-dives precipitously at about 75 months (or sometimes 55 months). So, Table 1: ![file] Fig 1D: ![file] ,
Keeping the world at hand: rapid visuomotor processing for hand–object interactions
Authors: Claudio Brozzoli
Tamar R Makin
Alessandro Farnè
Nicholas P Holmes
Journal: Experimental Brain Research (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: hand-centred visual processing; macaque premotor cortex; sensory guidance; object avoidance movements; manual actions
Affiliations: FMRIB Centre, Oxford University, Oxford, OX3 9DU, UK. 

Abstract:  The existence of hand-centred visual processing has long been established in the macaque premotor cortex. These hand-centred mechanisms have been thought to play some general role in the sensory guidance of movements towards objects, or, more recently, in the sensory guidance of object avoidance movements. We suggest that these hand-centred mechanisms play a specific and prominent role in the rapid selection and control of manual actions following sudden changes in the properties of the objects relevant for hand-object interactions. We discuss recent anatomical and physiological evidence from human and non-human primates, which indicates the existence of rapid processing of visual information for hand-object interactions. This new evidence demonstrates how several stages of the hierarchical visual processing system may be bypassed, feeding the motor system with hand-related visual inputs within just 70 ms following a sudden event. This time window is early enough, and this processing rapid enough, to allow the generation and control of rapid hand-centred avoidance and acquisitive actions, for aversive and desired objects, respectively. 

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: Another non-systematic, selective review. This one puts our TMS work in a wider context. (Systematic) reviews should be done to answer questions, rather than to interpret and or promote our own work. ,