PReD-Bench/PRed-Bench huggingface dataset:
Long non-coding RNA CASC15 promotes nasopharyngeal carcinoma cell proliferation and metastasis by downregulating miR-101-3p
Authors: M-Y Xue
H-X Cao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Nasopharyngeal carcinoma; long non-coding RNAs; lncRNA CASC15; tumorigenesis; Real Time-quantitative Polymerase Chain Reaction
Affiliations: Department of Otorhinolaryngology-Head and Neck Surgery, Affiliated Hospital of Jiangnan University (The Fourth People's Hospital of Wuxi), Wuxi, China. .

Abstract:  Objective: Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) play important roles in the progression of tumorigenesis. The aim of this study was to identify the exact role of lncRNA CASC15 in the progression of NPC. Patients and methods: CASC15 expression in both 54 paired NPC patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of CASC15 was identified by performing cell proliferation assay, transwell assay and wound healing assay in vitro. The underlying mechanism was explored through Luciferase assay and RT-qPCR. In addition, tumor formation and metastasis assays were conducted in vivo. Results: CASC15 expression in NPC tissues was markedly higher than that of adjacent non-tumor tissues. The proliferation, migration and invasion of NPC cells were significantly inhibited after knockdown of CASC15 in vitro. Our further experiments revealed that miR-101-3p was remarkably up-regulated via knockdown of CASC15. Meanwhile, miR-101-3p was a direct target of CASC15 in NPC. Furthermore, tumor formation and metastasis of NPC were significantly inhibited via knockdown of CASC15 in nude mice. Conclusions: CASC15 enhances NPC cell proliferation and metastasis via sponging miR-101-3p in vitro and in vivo. 

Retracted: Yes

PubPeer comments:
 **Table1, in addition to the data errors, the differentiation degree of HCC was directly divided into two groups according to well-moderate group and moderate-low group. In fact, in the pathological diagnosis report of tumor specimens, this kind of classification is impossible because pathologists simply describe the degree of tumor differentiation as well grade, moderate grade and low grade. So, how can the authors group the moderately differentiated HCC? This is a qualitative problem, not a quantitative one.** ![file] Just like the BCLC stage above. How can you put Stage A and Stage B into the same group? How can you put Stage B and Stage C into the same group? ,
Precise determination of graphene functionalization by in situ Raman spectroscopy
Authors: Andreas Hirsch
Herwig Peterlik
Philipp Vecera
Julio C Chacón-Torres
Konstantin Edelthalhammer
Himadri R Soni
Andreas Görling
Thomas Pichler
Stephanie Reich
Frank Hauke
Journal: Nature communications (2017)
Discipline: Multidisciplinary
Keywords: covalent functionalization; Raman spectroscopy; graphene; carbon allotropes; in situ study
Affiliations: Chair of Organic Chemistry II and Joint Institute of Advanced Materials and Processes (ZMP), Friedrich-Alexander University of Erlangen-Nuremberg, Henkestrasse 42, 91054 Erlangen, Germany., Institut für Experimental Physik, Freie Universität Berlin, Arnimallee 14, 14195 Berlin, Germany., Yachay Tech University, School of Physical Sciences and Nanotechnology, Urcuquí 100119, Ecuador., Faculty of Physics, University of Vienna, Strudlhofgasse 4, A-1090 Vienna, Austria., Chair of Theoretical Chemistry, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Egerlandstraße 3, 91058 Erlangen, Germany.

Abstract:  The verification of a successful covalent functionalization of graphene and related carbon allotropes can easily be carried out by Raman spectroscopy. Nevertheless, the unequivocal assignment and resolution of individual lattice modes associated with the covalent binding of addends was elusive up to now. Here we present an in situ Raman study of a controlled functionalization of potassium intercalated graphite, revealing several new bands appearing in the D-region of the spectrum. The evolution of these bands with increasing degree of functionalization from low to moderate levels provides a basis for the deconvolution of the different components towards quantifying the extent of functionalization. By complementary DFT calculations we were able to identify the vibrational changes in the close proximity of the addend bearing lattice carbon atoms and to assign them to specific Raman modes. The experimental in situ observation of the developing functionalization along with the reoxidation of the intercalated graphite represents an important step towards an improved understanding of the chemistry of graphene. 

Retracted: No

PubPeer comments:
 The numerical results presented in this paper are not reliable. For example, the reported optimal solution in Step 7 to (M2) is $$w=(0.2, 0.1, 0.3, 0.35)$$ **It is not even a feasible solution** because $$0.2 + 0.1 + 0.3 +0.35 = 0.95 1$$ Moreover, the requirements are not satisfied for $$0.25 le w_1 le 0.3$$ $$0.2 le w_2 le 0.25$$ Can the authors address this issue? ![file] ![file] ![file] ,
Bradykinin B2 Receptors of dendritic cells, acting as sensors of kinins proteolytically released by Trypanosoma cruzi, are critical for the development of protective type-1 responses
Authors: Ana Carolina Monteiro
Werner Müller-Esterl
Herbert B Tanowitz
Luciana Barros de Arruda
Fnu Nagajyothi
Verônica Schmitz
Alessandra Granato
Alexandre Morrot
João B Pesquero
Julio Scharfstein
Journal: PLoS Pathogens (2007)
Discipline: MICROBIOLOGY
Keywords: dendritic cells; Toll-like receptors; Trypanosoma cruzi; bradykinin B2 receptors; parasitemia
Affiliations: Instituto de Biofisica Carlos Chagas Filho, UFRJ, Rio de Janeiro, Brazil.

Abstract:  Although the concept that dendritic cells (DCs) recognize pathogens through the engagement of Toll-like receptors is widely accepted, we recently suggested that immature DCs might sense kinin-releasing strains of Trypanosoma cruzi through the triggering of G-protein-coupled bradykinin B2 receptors (B2R). Here we report that C57BL/6.B2R-/- mice infected intraperitoneally with T. cruzi display higher parasitemia and mortality rates as compared to B2R+/+ mice. qRT-PCR revealed a 5-fold increase in T. cruzi DNA (14 d post-infection [p.i.]) in B2R-/- heart, while spleen parasitism was negligible in both mice strains. Analysis of recall responses (14 d p.i.) showed high and comparable frequencies of IFN-gamma-producing CD4+ and CD8+ T cells in the spleen of B2R-/- and wild-type mice. However, production of IFN-gamma by effector T cells isolated from B2R-/- heart was significantly reduced as compared with wild-type mice. As the infection continued, wild-type mice presented IFN-gamma-producing (CD4+CD44+ and CD8+CD44+) T cells both in the spleen and heart while B2R-/- mice showed negligible frequencies of such activated T cells. Furthermore, the collapse of type-1 immune responses in B2R-/- mice was linked to upregulated secretion of IL-17 and TNF-alpha by antigen-responsive CD4+ T cells. In vitro analysis of tissue culture trypomastigote interaction with splenic CD11c+ DCs indicated that DC maturation (IL-12, CD40, and CD86) is controlled by the kinin/B2R pathway. Further, systemic injection of trypomastigotes induced IL-12 production by CD11c+ DCs isolated from B2R+/+ spleen, but not by DCs from B2R-/- mice. Notably, adoptive transfer of B2R+/+ CD11c+ DCs (intravenously) into B2R-/- mice rendered them resistant to acute challenge, rescued development of type-1 immunity, and repressed TH17 responses. Collectively, our results demonstrate that activation of B2R, a DC sensor of endogenous maturation signals, is critically required for development of acquired resistance to T. cruzi infection. 

Retracted: No

PubPeer comments:
 Figure 5. Much more similar than expected. https: imgur.com Z9CYJKX ,
Enhancing glass-forming ability via frustration of nano-clustering in alloys with a high solvent content
Authors: M K Miller
A D Stoica
D Ma
X L Wang
Z B Jiao
Z P Lu
H X Li
Y Ren
Y Wu
J E Gao
Journal: Scientific Reports (2013)
Discipline: Multidisciplinary
Keywords: Glass-forming ability; Alloys; Fe-based; Al-based; Saturation magnetization
Affiliations: State Key Laboratory for Advanced Metals and Materials, University of Science and Technology Beijing, Beijing 100083, China.

Abstract:  The glass-forming ability (GFA) of alloys with a high-solvent content such as soft magnetic Fe-based and Al-based alloys is usually limited due to strong formation of the solvent-based solid solution phase. Herein, we report that the GFA of soft magnetic Fe-based alloys (with &gt;70 at.% Fe to ensure large saturation magnetization) could be dramatically improved by doping with only 0.3 at.% Cu which has a positive enthalpy of mixing with Fe. It was found that an appropriate Cu addition could enhance the liquid phase stability and crystallization resistance by destabilizing the α-Fe nano-clusters due to the necessity to redistribute the Cu atoms. However, excessive Cu doping would stimulate nucleation of the α-Fe nano-clusters due to the repulsive nature between the Fe and Cu atoms, thus deteriorating the GFA. Our findings provide new insights into understanding of glass formation in general. 

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. , 
 In addition to the finding in figure 4 above, with which I agree, there seems also to be a repeated image between figures 4 and 5 (yellow boxes). Red box and ellipse in original. *** ![file] *** ![file] ,
Effects of microRNA-146a on the proliferation and apoptosis of human osteoarthritis chondrocytes by targeting TRAF6 through the NF-κB signalling pathway
Authors: Jun-Hua Zhong
Shu-Yi Yan
Yong-Bing Zhang
Cui-Fang Liu
Rui-Xiang Bian
Shou-Mei Zhao
Ning Liu
Jing Li
Journal: Bioscience Reports (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Chondrocyte; MicroRNA-146a; NF-κB signaling pathway; Osteoarthritis; Proliferation
Affiliations: Department of Surgery, Dongying People’s Hospital, Dongying 257091, P.R. China, Department of Joint Surgery, Dongying People’s Hospital, Dongying 257091, P.R. China

Abstract:  The present study aims to investigate the effects of miR-146a on the proliferation and apoptosis of human osteoarthritis (OA) chondrocytes by targeting tumour necrosis factor receptor-associated factor 6 (TRAF6) through nuclear factor-κB (NF-κB) signalling pathway. Human normal and OA chondrocytes were selected and divided into the normal group, blank group, negative control (NC) group, miR-146a mimics group, miR-146a inhibitors, miR-146a inhibitor + si-TRAF6 group and si-TRAF6 group. Quantitative real-time PCR (qRT-PCR) was applied to detect the expressions of miR-146a, TRAF6 mRNA and NF-κB mRNA. Western blotting was used to detect the protein expressions of TRAF6 and NF-κB. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis. Compared with normal chondrocytes, the expression of miR-146a decreased, while the mRNA and protein expressions of TRAF6 and NF-κB increased in OA chondrocytes. OA chondrocytes had a lower proliferation rate and a higher apoptosis rate than the normal chondrocytes. Compared with the blank, NC and si-TRAF6 groups, the expression of miR-146a increased in the miR-146a mimics group, but decreased in the miR-146a inhibitors and miR-146a inhibitor + si-TRAF6 groups. Compared with the blank, NC and miR-146a inhibitor + si-TRAF6 groups, the mRNA and protein expressions of TRAF6 and NF-κB decreased, cell proliferation rate increased and cell apoptosis rate decreased in the miR-146a mimics and si-TRAF6 groups, while opposite trends were observed in the miR-146a inhibitors group. Our study suggests that miR-146a could promote proliferation and inhibit apoptosis of OA chondrocytes by inhibiting TRAF6 expression and suppressing the activation of NF-κB signalling pathway. 

Retracted: No

PubPeer comments:
 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. , 
 #1 Original thread here: https: pubpeer.com publications 55115A422D4E04E396DBA657511D12 ,
Hostility predicts mortality but not recurrent acute coronary syndrome
Authors: Kathleen Dracup
Tracey K Vitori
Debra K Moser
Martha J Biddle
Susan K Frazier
Michele M Pelter
Gia Mudd-Martin
Journal: European Journal of Cardiovascular Nursing (2020)
Discipline: CLINICAL MEDICINE
Keywords: Hostility; acute coronary syndrome; cardiovascular disease.
Affiliations: University of Tennessee College of Nursing, USA, University of Kentucky College of Nursing, USA, University of California, San Francisco, USA

Abstract:  Background: Hostility is associated with greater risk for cardiac disease, cardiac events and dysrhythmias. Investigators have reported equivocal findings regarding the association of hostility with acute coronary syndrome (ACS) recurrence and mortality. Given mixed results on the relationship between hostility and cardiovascular outcomes, further research is critical. Aims: The aim of our study was to determine whether hostility was a predictor of ACS recurrence and mortality. Methods: We performed a secondary analysis of data (N = 2321) from a large randomized clinical trial of an intervention designed to reduce pre-hospital delay among patients who were experiencing ACS. Hostility was measured at baseline with the Multiple Adjective Affect Checklist (MAACL) and patients were followed for 24 months for evaluation of ACS recurrence and all-cause mortality. We used Cox proportional hazards modeling to determine whether hostility was predictive of time to ACS recurrence or all-cause mortality. Results: The majority of patients were married (73%), Caucasian (97%), men (68%), and had a mean age of 67 ± 11 years. Fifty-seven percent of participants scored as hostile based on the established MAACL cut point (mean score = 7.56 ± 3.8). Hostility was an independent predictor of all-cause mortality (p = &lt; 0.039), but was not a predictor of ACS recurrence (p = 0.792). Conclusion: Hostility is common in patients with ACS and its relationship to clinical outcomes is important to the design of future interventions to improve long-term ACS mortality. 

Retracted: No

PubPeer comments:
 Data from Figure 4 is reused in a problematic Figure from 2015: ![file] , 
 In figure 3, a strip of colonies was used twice for different conditions. ![file] , 
 Figure 4C contains background duplication. ![file] , 
 In Figure 6A the same band is used for L3 AtTUB6 and for L1 CsMTP8 ![file] , 
 Retracted: https: academic.oup.com jxb advance-article doi 10.1093 jxb erz449 5714919 ,
Investigation of antioxidant, anti-inflammatory and DNA-protective properties of eugenol in thioacetamide-induced liver injury in rats
Authors: Baskaran Yogalakshmi
Periyasamy Viswanathan
Carani Venkatraman Anuradha
Journal: Toxicology (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: eugenol; thioacetamide; hepatic injury; rats; liver injury
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608 002, Tamil Nadu, India.

Abstract:  The present study investigated the preventive effect of eugenol, a naturally occurring food flavouring agent on thioacetamide (TA)-induced hepatic injury in rats. Adult male Wistar rats of body weight 150-180 g were used for the study. Eugenol (10.7 mg/kg b.w./day) was administered to rats by oral intubation for 15 days. TA was administered (300 mg/kg b.w., i.p.) for the last 2 days at 24h interval and the rats were sacrificed on the 16th day. Markers of liver injury (aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma-glutamyl transferase and bilirubin), inflammation (myeloperoxidase, tumor necrosis factor-alpha and interleukin-6), oxidative stress (lipid peroxidation indices, protein carbonyl and antioxidant status) and cytochrome P4502E1 activity were assessed. Expression of cyclooxygenase-2 (COX-2) and the extent of DNA damage were analyzed using immunoblotting and comet assay, respectively. Liver injury and collagen accumulation were assessed using histological studies by hematoxylin and eosin and Masson trichrome staining. Rats exposed to TA alone showed increased activities of hepatocellular enzymes in plasma, lipid peroxidation indices, inflammatory markers and pro-inflammatory cytokines and decreased antioxidant status in circulation and liver. Hepatic injury and necrosis were also evidenced by histology. Eugenol pretreatment prevented liver injury by decreasing CYP2E1 activity, lipid peroxidation indices, protein oxidation and inflammatory markers and by improving the antioxidant status. Single-cell gel electrophoresis revealed that eugenol pretreatment prevented DNA strand break induced by TA. Increased expression of COX-2 gene induced by TA was also abolished by eugenol. These findings suggest that eugenol curtails the toxic effects of TA in liver. 

Retracted: No

PubPeer comments:
 This article appears to be computer-generated with [SCIgen] . ![file] --- This comment was written by Guillaume Cabanac and Cyril Labbu00e9. Contact: [SeekAndBlastn-Operators@univ-grenoble-alpes.fr](mailto:SeekAndBlastn-Operators@univ-grenoble-alpes.fr). ,
MiR-1294 acts as a tumor suppressor in clear cell renal cell carcinoma through targeting HOXA6
Authors: Y Wu
H-L Cai
J-C Fang
W Pan
L-J Pang
W Zhang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Renal cancer; clear cell renal cell carcinoma; microRNAs; miR-1294; progression
Affiliations: Department of Urinary Surgery, RenMin Hospital of Huangpi District, the Third Hospital of Jianghan University, Huangpi District, Wuhan, P. R. China. .

Abstract:  Objective: Renal cancer represents about 3% of all human cancers. Clear cell renal cell carcinoma (ccRCC) is the main type of renal cancer. MicroRNAs (miRNAs) have been reported to play crucial roles in the carcinogenesis of human cancers. This study was aimed to investigate the expression of miR-1294 and the mechanisms underlying miR-1294-mediated ccRCC progression. Materials and methods: The miR-1294 expression levels in ccRCC cell lines were analyzed by quantified real time-PCR (qRT-PCR). The effect of the miR-1294 expression on the overall survival of ccRCC patients was analyzed by the Kaplan-Meier Plotter. Cell proliferation, colony growth, and cell invasion were examined by cell counting kit-8 assay, colony formation assay, and transwell invasion assay, respectively. The luciferase activity reporter assay and Western blot assay were conducted to validate the connection between miR-1294 and homeobox A6 (HOXA6). Results: MiR-1294 was downregulated in ccRCC cell lines and correlated with the poor overall survival of ccRCC patients. The overexpression of miR-1294 inhibits ccRCC cell proliferation, colony growth, and cell invasion. HOXA6 was validated as a target of miR-1294 and negatively regulated by miR-1294. The overexpression of HOXA6 attenuated the miR-1294-mediated effects on ccRCC cellular functions. Conclusions: Our results indicated that miR-1294 functions as a tumor suppressor in ccRCC. MiR-1294 suppressed cell proliferation, colony formation, and invasion in ccRCC partially via targeting HOXA6. 

Retracted: No

PubPeer comments:
 Figure 2D. Two of the panels appear to show some repetitive features. Boxes of the same color focus attention to some of these similarities. ![file] , 
 The Western blots in this paper appear to share similar background patterns. This problem has also been observed in a large set of papers described in a January 2020 post on Leonid Schneider s blog: https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers , although the backgrounds in the blots in this paper are different and of a higher resolution. For example, here are two sets of blots from Figure 3C. The left 2 blots show different proteins and differently shaped bands, but the backgrounds are remarkably similar. The right 2 blots also share very similar backgrounds, albeit different than the one in the left 2 blots. Boxes of the same color draw attention to some of these background areas that share similarities. ![file] ,
Emergence of carbapenemase-producing and colistin resistant Klebsiella pneumoniae ST101 high-risk clone in Turkey
Authors: Gülşen Hazırolan
Alper Karagöz
Journal: Acta Microbiologica et Immunologica Hungarica (2020)
Discipline: MICROBIOLOGY
Keywords: Klebsiella pneumoniae; MLST; PFGE; ST101; ST147
Affiliations: 1Department of Medical Microbiology, Faculty of Medicine, Hacettepe University, 06100, Ankara, Turkey., 2Department of Microbiology, Faculty of Molecular Biology and Genetics, Usak University, 64200, Usak, Turkey.

Abstract:  Carbapenemase-producing and colistin resistant Klebsiella pneumoniae has become a worldwide healthcare problem. This study describes molecular characterization of carbapenemase-producing and colistin resistant clinical K. pneumoniae isolates.A total of 93 non-replicate carbapenem and colistin resistant K. pneumoniae were recovered from clinical specimens in a university hospital during 2017-2019. Detection of blaOXA-48, blaKPC, blaNDM-1, blaIMP, blaVIM-1 and mcr-1, -2, -3, -4, -5, -6, -7, and -8 genes was performed by PCR. The bacterial isolates were assigned to clonal lineages by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST).All isolates harbored blaOXA-48 and only two isolates harbored blaOXA-48, and blaNDM-1 genes together. In colistin resistant K. pneumoniae, mcr-1 was detected in two (2.1%) isolates. Ninety three isolates of K. pneumoniae were categorized into three clusters and five pulsotypes. MLST revealed two different sequence types, ST101 (89/93) and ST147 (4/93).In our study ST101 was found to be a significantly dominant clone carrying blaOXA-48 and among our strains a low frequency of mcr-1 gene was determined. The emergence of colistin resistance was observed in K. pneumoniae ST101 isolates. ST101 may become a global threat in the dissemination of carbapenem and colistin resistance. 

Retracted: No

PubPeer comments:
 Iu2019m confused by the *conflict of interest* disclosure when the *funding* disclosure explicitly states that the unnamed funder has an interest in the subject matter of this paper, namely yoga (see image below). Further, at least one of the researchers appears employed by the Chopra Foundation, which was founded and is chaired by Deepak Chopra who promotes u201cintegrative health,u201d in which meditation, yoga and other spiritual practices supplement conventional medicine. Source: https: blogs.scientificamerican.com cross-check my-doubts-about-deepak-chopra-and-the-monetization-of-meditation Could the authors update the COI disclosure to either identify the funder so readers can judge the independence of the research performed, or to more clearly indicate the potentially close relationship between the authors employer(s) and the commercial ties aimed at promoting the benefits of yoga. Failure to make this explicit disclosure seems atypical for research papers. *** ![file] , 
 Another test, sorry for any inconvenience.... Will delete soon(ish). ,
Overexpression of Rab25 contributes to metastasis of bladder cancer through induction of epithelial–mesenchymal transition and activation of Akt/GSK-3β/Snail signaling
Authors: Fang Zheng
Jian Lu
Bin Yu
Junhang Luo
Xiaoxia Huang
Wei Chen
Zhuting Tong
Bing Liao
Jinhuan Wei
Yong Fang
Jiaxing Zhang
Zhenhua Chen
Bin Li
Dan Xie
Journal: Carcinogenesis (2013)
Discipline: CLINICAL MEDICINE
Keywords: Rab25; bladder cancer; metastasis; epithelial-mesenchymal transition; Akt
Affiliations: Department of Urology and.

Abstract:  Rab25, an epithelial-specific member of the Rab family of small guanosine triphosphatases, is associated with several human cancers. The goal of this study was to determine its function in bladder cancer (BC). We examined the Rab25 expression pattern in two different cohorts of BC patients treated with radical cystectomy by quantitative PCR, western blotting and immunohistochemical staining. A series of in vitro and in vivo assays were performed to elucidate the function of Rab25 in BC and its underlying mechanisms. Rab25 expression was significantly elevated at both the messenger RNA and protein levels in BCs compared with normal bladder tissues. High Rab25 expression was closely associated with lymph node (LN) metastasis and was an independent predictor for poor disease-free survival in BC patients. Downregulation of Rab25 in BC cells markedly inhibited invasive motility in vitro and metastatic potential in vivo. In addition, downregulation of Rab25 in BC EJ and T24 cells increased the expression levels of epithelial markers (E-cadherin and α-catenin) and decreased the levels of mechamechy markers (vimentin and fibronectin). Simultaneously, downregulation of Rab25 in EJ and T24 cells resulted in the inactivation of downstream phosphorylated protein kinase B (p-Akt), phosphorylated glycogen synthase kinase-β (p-GSK-3β) and snail signaling. This study demonstrates that Rab25 can promote BC metastasis through induction of epithelial-mesenchymal transition process and activation of Akt/GSK-3β/Snail signaling pathway; Rab25 expression level can predict LN metastasis and inferior clinical outcome in BC patients. 

Retracted: No

PubPeer comments:
 There was a overlap in fig3d.![file] , 
 #1 The overlap appears to extend to the top of the images. *** ![file] *** Also, an apparent repeated image in Figure 4B, with slightly different contrast brightness. ![file] , 
 I would also note for other readers that this group appears to have more than a [dozen papers] with similar concerns. ,
Laser immunotherapy with gold nanorods causes selective killing of tumour cells
Authors: Rejiya C S
Annie Abraham
Raji V
Vibin M
Jatish Kumar
Journal: Pharmacological Research (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Nanoparticles; Cancer therapeutics; Gold nanorods; Anti-cancer potential; Laser light
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom Campus, Thiruvananthapuram, Kerala, India.

Abstract:  Therapeutic approaches that exploit nanoparticles to deliver drugs selectively to cancer cells are currently considered one of the most promising avenues in the area of cancer therapeutics. Recently, gold nanorods (AuNRs) have shown promising biological applications due to their unique electronic and optical properties. In this paper, we have demonstrated the anti-cancer potential of gold nanorods with low power laser light. Gold nanorods (AuNRs), surface modified with poly (styrene sulfonate) PSS and functionalized with epidermal growth factor receptor antibody conjugated with gold nanorods (anti-EGFR-AuNRs) were successfully synthesised and characterized by UV-Visible-NIR spectrophotometry and High Resolution Transmission Electron Microscopy (HR-TEM). Inductively Coupled Plasmon Atomic Emission Spectrometry (ICP-AES) and Immunofluorescence studies confirmed the efficient uptake of these functionalized gold nanorods by human squamous carcinoma cells, A431. The in vitro photothermal therapy was conducted in four groups - control, laser alone, unconjugated AuNRs with laser and anti-EGFR conjugated AuNRs with laser. Phase contrast images have revealed cell morphology changes and cell death after the laser irradiation. In order to determine whether the cell death occur due to apoptosis or necrosis, we have evaluated the biochemical parameters such as lactate dehydrogenase release, reactive oxygen species level, mitochondrial membrane potential and caspase-3 activity. Flow cytometry analysis have shown the cell cycle changes after laser irradiation with antibody conjugated gold nanorods. Thus the results of our experiments confirmed that immunolabeled gold nanorods can selectively destruct the cancer cells and induce its apoptosis through ROS mediated mitochondrial pathway under low power laser exposure. 

Retracted: No

PubPeer comments:
 Could the authors clarify these problematic images in their two publications??? ![file] ![file] ![file] , 
 I came here to post a similar comment about Figure 1. As Saxifraga Brunonis already hinted at in their comment #1, panels A (Unconjugated AuNRs) and C (anti-EGFR conjugated AuNRs ) appear to show the same sample, albeit zoomed in differently. Here is a different illustration to make that more clear: ![file] ,
Post-transcriptional control of catalase expression in garlic-treated rats
Authors: M D Granados-Silvestre
P D Maldonado
M E Ibarra-Rubio
J Pedraza-Chaverrí
O N Medina-Campos
I M Olivares-Corichi
Journal: Molecular and Cellular Biochemistry (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Catalase; Garlic; Antioxidant enzyme; Oxidative stress; mRNA levels
Affiliations: Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico UNAM, México.

Abstract:  Regulation of catalase (CAT) expression, a major antioxidant enzyme that detoxifies H2O2, is very complex. Garlic is effective to prevent or ameliorate oxidative stress probably through its intrinsic antioxidant properties and/or to its ability to modify antioxidant enzyme expression. In this paper we studied the effect of a 2% garlic diet on the renal and hepatic CAT expression (mRNA levels, and enzyme activity, content, synthesis, and degradation). The study was made 2 weeks after feeding rats with a 2% garlic diet. CAT activity and content were measured by a spectrophotometric method and Western blot, respectively. CAT mRNA levels and CAT synthesis (k(s)) and degradation (kD) in vivo were measured by Northern blot and kinetic of reappearance of CAT activity after aminotriazole injection, respectively. Garlic-treatment decreased CAT activity and content, and CAT mRNA levels were unchanged in both tissues. k(s) decreased and kD remained unchanged in kidney and liver. The decrease in k(s) without changes in kD and CAT mRNA levels could explain the low CAT expression in garlic-fed rats. In vivo H2O2 generation in kidney and liver was markedly decreased in garlic-fed rats which could be due to a direct antioxidant effect of garlic. This may be the initial event in the garlic-fed rats that leads to the decreased CAT expression. Our data strongly suggest that the diminished renal and hepatic CAT expression in garlic-fed rats is mediated by post-transcriptional changes (mainly low translational efficiency) which could be an adaptation to the low H2O2. 

Retracted: No

PubPeer comments:
 For a critique of this study see: http: deevybee.blogspot.com 2019 01 neuropointdxs-blood-test-for-autism.html ,
Long non‐coding RNA TCONS_00041960 enhances osteogenesis and inhibits adipogenesis of rat bone marrow mesenchymal stem cell by targeting miR‐204‐5p and miR‐125a‐3p
Authors: Xuefeng Zhao
Xiaoya Sun
Yadong Wang
Guoqiang Zhao
Yuebai Li
Yisheng Wang
Hongya Guan
Yan Xu
Shanfeng Zhang
Guowei Shang
Journal: Journal of Cellular Physiology (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LncRNA TCONS_00041960; bone marrow mesenchymal stem cells; differentiation; miR-125a-3p; miR-204-5p.
Affiliations: Department of Orthopaedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China., Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China., Department of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.

Abstract:  A growing number of long non-coding RNAs (lncRNAs) have been found to be involved in diverse biological processes such as cell cycle regulation, embryonic development, and cell differentiation. However, limited knowledge is available concerning the underlying mechanisms of lncRNA functions. In this study, we found down-regulation of TCONS_00041960 during adipogenic and osteogenic differentiation of glucocorticoid-treated bone marrow mesenchymal stem cells (BMSCs). Furthermore, up-regulation of TCONS_00041960 promoted expression of osteogenic genes Runx2, osterix, and osteocalcin, and anti-adipogenic gene glucocorticoid-induced leucine zipper (GILZ). Conversely, expression of adipocyte-specific markers was decreased in the presence of over-expressed TCONS_00041960. Mechanistically, we determined that TCONS_00041960 as a competing endogenous RNA interacted with miR-204-5p and miR-125a-3p to regulate Runx2 and GILZ, respectively. Overall, we identified a new TCONS_00041960-miR-204-5p/miR-125a-3p-Runx2/GILZ axis involved in regulation of adipogenic and osteogenic differentiation of glucocorticoid-treated BMSCs. 

Retracted: No

PubPeer comments:
 Figure 2(f); Fig 5(i).  Oil red O staining was performed at day 14. Considerable overlap between panels depicting different treatments. ![file]  Dex condition = 1u00d710-6 mol L dexamethasone. , 
 It would be useful to know whether the BMSCs in the repeated panel here were Oil-stained after culturing for 0 days, as in Figure 1(a) *[left]*, or after 14 days, as in Fig 5(i) *[right]*. ![file] , 
 [Perhaps a systemic problem] . Journals and readers may wish to proceed with caution. ,
Mycobacterium indicus pranii induces dendritic cell activation, survival, and Th1/Th17 polarization potential in a TLR-dependent manner
Authors: Soumitra Marathe
Vini John
Sangeeta Bhaskar
Gobardhan Das
Pawan Kumar
Journal: Journal of Leukocyte Biology (2015)
Discipline: IMMUNOLOGY
Keywords: T cell polarization; apoptosis; costimulatory molecules; cytokines; pattern recognition receptors.
Affiliations: *National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India., *National Institute of Immunology, New Delhi, India; and International Centre for Genetic Engineering and Biotechnology, New Delhi, India .

Abstract:  MIP is a nonpathogenic, soil-borne predecessor of Mycobacterium avium. It has been reported previously that MIP possesses strong immunomodulatory properties and confers protection against experimental TB and tumor. DCs, by virtue of their unmatched antigen-presentation potential, play a critical role in activation of antitumor and antimycobacterial immune response. The effect of MIP on the behavior of DCs and the underlying mechanisms, however, have not been investigated so far. In the present study, we showed that MIP induces significant secretion of IL-6, IL-12p40, IL-10, and TNF-α by DCs and up-regulates the expression of costimulatory molecules CD40, CD80, and CD86. MIP(L) induced a significantly higher response compared with MIP(K). PI and Annexin V staining showed that MIP increases DC survival by inhibiting apoptosis. Consistently, higher expression of antiapoptotic proteins Bcl-2 and Bcl-xl was observed in MIP-stimulated DCs. Cytokines, produced by naïve T cells, cocultured with MIP-stimulated DCs, showed that MIP promotes Th1/Th17 polarization potential in DCs. Response to MIP was lost in MyD88(-/-)DCs, underscoring the critical role of TLRs in MIP-induced DC activation. Further studies revealed that TLR2 and TLR9 are involved in DC activation by MIP(L), whereas MIP(K) activates the DCs through TLR2. Our findings establish the DC activation by MIP, define the behavior of MIP-stimulated DCs, and highlight the role of TLRs in MIP-induced DC activation. 

Retracted: No

PubPeer comments:
 In equation 41, I believe the first term should be negative, as shown below. The $kappa$ term in equation 40 is negative. $$ frac{partial chi^{vp}}{partial Deltagamma^{vp}}= -frac{partial kappa}{partial Delta p} frac{partial Delta p}{partial Delta gamma^{vp}} -frac{sigma^{0}_{y}}{gamma^{vp}N} left( frac{Deltagamma^{vp}}{Delta tGamma^{vp}} right)^{1 N} $$ , 
 The indices in the partial derivative in equation 44 are incorrect. They should be swapped. The correct notation is shown below: $$ left(Deltasigma^t_{ij}right)^{k+1}= left(Deltasigma^t_{ij}right)^{k}- left[left( frac{partial R^t_{kl}}{partialsigma^t_{ij}} right)^kright]^{-1} left(R^t_{kl}right)^k $$ ,
Hypoxia-Induced Autophagy Enhances Cisplatin Resistance in Human Bladder Cancer Cells by Targeting Hypoxia-Inducible Factor-1α
Authors: Kefeng Ding
Nanzhang
Jiaquao Xiao
Xiawa Mao
Huifeng Wu
Journal: Journal of Immunology Research (2021)
Discipline: IMMUNOLOGY
Keywords: Hypoxia; Chemoresistance; Bladder cancer cells; Autophagy; Cisplatin
Affiliations: Urology Department, The 2nd Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, Zhejiang Province 310000, China., Oncology Department, The 2nd Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, Zhejiang Province 310000, China.

Abstract:  Purpose: To investigate the effect of hypoxia on chemoresistance and the underlying mechanism in bladder cancer cells. Methods: BIU-87 bladder cancer cell line was treated with cisplatin under hypoxic and normoxic conditions and tested using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and Western blotting. All the data were expressed as mean ± standard error from three independent experiments and analyzed by multiple t-tests. Results: Apoptosis of bladder cancer cells caused by cisplatin was attenuated in hypoxic conditions. Hypoxia enhanced autophagy caused by cisplatin. The autophagy inhibitor and HIF-1α inhibitor can reverse the chemoresistance in hypoxic condition. Apoptosis and autophagy of bladder cancer cells were downregulated by HIF-1α inhibitor YC-1. Hypoxia-induced autophagy enhanced chemoresistance to cisplatin via the HIF-1 signaling pathway. Conclusion: Resistance to cisplatin in BIU-87 bladder cancer cells under hypoxic conditions can be explained by activation of autophagy, which is regulated by HIF-1α-associated signaling pathways. The hypoxia-autophagy pathway may be a target for improving the efficacy of cisplatin chemotherapy in bladder cancer. 

Retracted: No

PubPeer comments:
 This paper makes use of the  BIU-87 bladder cancer cell line . Unfortunatly it has been shown that BIU-87 is probably not a human cell line. Its origin is not clear, but it can not be used as a model of bladder cancer. Thus the conclusions of this paper as relevant to bladder cancers are most probably incorrect. See the relevant [Cellosaurus entry] , 
 #1 Deer Amos Bairoch Thank you for your comments. In your opinion BIU-87 bladder cell line is not a pure human cell line and we cannot take it for our study. However so far, BIU87 cells are thought to have originated from human tumor cells. And many experiments have used this cell line to draw relevant conclusions.[1] In the following experiment we are using two cell lines for the next experiment, including BIU-87 and T24. 1: Lu N, Piao MH, Feng CS, Yuan Y. Isoflurane promotes epithelial-to-mesenchymal transition and metastasis of bladder cancer cells through HIF-1u03b1-u03b2-catenin Notch1 pathways. Life Sci. 2020 Oct 1;258:118154. ,
Targeting TPX2 suppresses proliferation and promotes apoptosis via repression of the PI3k/AKT/P21 signaling pathway and activation of p53 pathway in breast cancer
Authors: Yin Tong
Qian Ma
Hui Zheng
Miaomiao Chen
Yanchun Wang
Hongqin Zhang
Guihong Zhang
Ailing Zhong
Lin Guo
Renquan Lu
Suhong Xie
Jinyan Kai
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AKT signaling pathway; Breast cancer; Cell apoptosis; TPX2; p53.
Affiliations: Department of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China., Department of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China., Department of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address: .

Abstract:  Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is a microtubule-associated protein required for mitosis and spindle assembly. Previous studies showed that TPX2 is overexpressed in various human cancers and promotes cancer progression. In this study, the differentially expressed genes including TPX2 were screened in GEO database for gene expression microarray of breast cancer. The TPX2 expression level was significantly increased in breast cancer cells and the breast malignant tissues compared with those controls. In vitro experiment further confirmed that knockdown of TPX2 by small hairpin RNA inhibited breast cancer cell proliferatio, migration, and induced cell apoptosis. TPX2 silencing decreased the expression of PI3K and extent of AKT phosphorylation, as well as increased expression of p53 and p21. Taken together, our findings indicate that TPX2 silencing negatively regulates the PI3K/AKT and activates p53 signaling pathway by which breast cancer cells proliferation were inhibited whereas cellulars apoptosis were accelerated, suggesting that TPX2 may be a potential target for anticancer therapy in breast cancer. 

Retracted: No

PubPeer comments:
 Figure 2C appears to have a repeated image, with different resolution and after 90 degree rotation. *** ![file] ,
The study of endogenous hepatocyte growth factor in the pathogenesis of intracranial aneurysms
Authors: Z-H Wang
Y-J Liu
L-X Liu
L-L Yu
L Shi
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: endogenous; hepatocyte growth factor; pathogenesis; intracranial aneurysms; withdrawn
Affiliations: Department of Neurosurgery, Qingdao Hiser Medical Center, Qingdao, Shandong, China.

Abstract:  The article "The study of endogenous hepatocyte growth factor in the pathogenesis of intracranial aneurysms" by L.-L. Yu, Y.-J. Liu, Z.-H. Wang, L. Shi, L.-X. Liu, published in Eur Rev Med Pharmacol Sci 2017; 21 (4): 795-803 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
Small Extracellular Vesicle Regulation of Mitochondrial Dynamics Reprograms a Hypoxic Tumor Microenvironment
Authors: Lucia R Languino
Shiv Ram Krishn
Jun Qin
Edward F Plow
Andrew V Kossenkov
Irene Bertolini
Jagadish C Ghosh
Sudheer Mulugu
Valentina Vaira
Dario C Altieri
Journal: Developmental Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: breast cancer; extracellular vesicles; hypoxia; mitochondria; morphogenesis
Affiliations: Prostate Cancer Discovery and Development Program, The Wistar Institute, Philadelphia, PA 19104, USA; Immunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA., Center for Systems and Computational Biology, The Wistar Institute, Philadelphia, PA 19104, USA., Electron Microscopy Resource Laboratory, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA., Prostate Cancer Discovery and Development Program, The Wistar Institute, Philadelphia, PA 19104, USA; Department of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA., Division of Pathology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan 20122, Italy; Department of Pathophysiology and Transplantation, University of Milan, Milan 20122, Italy., Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA., Prostate Cancer Discovery and Development Program, The Wistar Institute, Philadelphia, PA 19104, USA; Immunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA. Electronic address: .

Abstract:  The crosstalk between tumor cells and the adjacent normal epithelium contributes to cancer progression, but its regulators have remained elusive. Here, we show that breast cancer cells maintained in hypoxia release small extracellular vesicles (sEVs) that activate mitochondrial dynamics, stimulate mitochondrial movements, and promote organelle accumulation at the cortical cytoskeleton in normal mammary epithelial cells. This results in AKT serine/threonine kinase (Akt) activation, membrane focal adhesion turnover, and increased epithelial cell migration. RNA sequencing profiling identified integrin-linked kinase (ILK) as the most upregulated pathway in sEV-treated epithelial cells, and genetic or pharmacologic targeting of ILK reversed mitochondrial reprogramming and suppressed sEV-induced cell movements. In a three-dimensional (3D) model of mammary gland morphogenesis, sEV treatment induced hallmarks of malignant transformation, with deregulated cell death and/or cell proliferation, loss of apical-basal polarity, and appearance of epithelial-to-mesenchymal transition (EMT) markers. Therefore, sEVs released by hypoxic breast cancer cells reprogram mitochondrial dynamics and induce oncogenic changes in a normal mammary epithelium. 

Retracted: No

PubPeer comments:
 The control images in Figure 1C appear to be unexpectedly similar for difference cell lines, with an adjustment to brightness. There appear to be a number of papers by [common author ] with concerns. *** ![file] ,
Flux-induced topological superconductivity in full-shell nanowires
Authors: B van Heck
S Vaitiekėnas
T Karzig
G W Winkler
P Krogstrup
L I Glazman
R M Lutchyn
K Flensberg
C Nayak
C M Marcus
M-T Deng
Journal: Science (2020)
Discipline: Multidisciplinary
Keywords: Hybrid semiconductor-superconductor nanowires; topological superconductivity; magnetic flux; induced gap; phase winding
Affiliations: Center for Quantum Devices and Microsoft Quantum Lab-Copenhagen, Niels Bohr Institute, University of Copenhagen, 2100 Copenhagen, Denmark., Microsoft Quantum, Microsoft Station Q, University of California, Santa Barbara, Santa Barbara, CA 93106, USA., Departments of Physics and Applied Physics, Yale University, New Haven, CT 06520, USA., Microsoft Quantum, Microsoft Station Q, University of California, Santa Barbara, Santa Barbara, CA 93106, USA.  ., Center for Quantum Devices and Microsoft Quantum Lab-Copenhagen, Niels Bohr Institute, University of Copenhagen, 2100 Copenhagen, Denmark.  .

Abstract:  Hybrid semiconductor-superconductor nanowires have emerged as a promising platform for realizing topological superconductivity (TSC). Here, we present a route to TSC using magnetic flux applied to a full superconducting shell surrounding a semiconducting nanowire core. Tunneling into the core reveals a hard induced gap near zero applied flux, corresponding to zero phase winding, and a gapped region with a discrete zero-energy state around one applied flux quantum, corresponding to 2π phase winding. Theoretical analysis indicates that the winding of the superconducting phase can induce a transition to a topological phase supporting Majorana zero modes. Measured Coulomb blockade peak spacing around one flux quantum shows a length dependence that is consistent with the existence of Majorana modes at the ends of the nanowire. 

Retracted: No

PubPeer comments:
 https: retractionwatch.com 2021 07 29 science-majorana-paper-earns-an-expression-of-concern ,