PReD-Bench/PRed-Bench huggingface dataset:
Clinical Effectiveness of Liposomal Bupivacaine Administered by Infiltration or Peripheral Nerve Block to Treat Postoperative Pain
Authors: Rodney A Gabriel
James C Eisenach
Brian M Ilfeld
Journal: Anesthesiology (2021)
Discipline: CLINICAL MEDICINE
Keywords: liposomal bupivacaine; postoperative pain; randomized controlled trials; Exparel; Pacira Pharmaceuticals

Abstract:  The authors provide a comprehensive summary of all randomized, controlled trials (n = 76) involving the clinical administration of liposomal bupivacaine (Exparel; Pacira Pharmaceuticals, USA) to control postoperative pain that are currently published. When infiltrated surgically and compared with unencapsulated bupivacaine or ropivacaine, only 11% of trials (4 of 36) reported a clinically relevant and statistically significant improvement in the primary outcome favoring liposomal bupivacaine. Ninety-two percent of trials (11 of 12) suggested a peripheral nerve block with unencapsulated bupivacaine provides superior analgesia to infiltrated liposomal bupivacaine. Results were mixed for the 16 trials comparing liposomal and unencapsulated bupivacaine, both within peripheral nerve blocks. Overall, of the trials deemed at high risk for bias, 84% (16 of 19) reported statistically significant differences for their primary outcome measure(s) compared with only 14% (4 of 28) of those with a low risk of bias. The preponderance of evidence fails to support the routine use of liposomal bupivacaine over standard local anesthetics. 

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2021 04 15 pharma-company-demands-retraction-damages-in-lawsuit-against-journal for concerns about this article. ,
A super-spreader of COVID-19 in Ningbo city in China
Authors: Kun Yan
Jie Lin
Ting Cai
Jianjun Zheng
Jingfeng Zhang
Journal: Journal of Infection and Public Health (2020)
Discipline: IMMUNOLOGY
Keywords: COVID19; Super-spreader; Virus features.
Affiliations: Hwa Mei Hospital, University of Chinese Academy of Sciences, China., Hwa Mei Hospital, University of Chinese Academy of Sciences, China; Institute of Life and Health Industry, University of Chinese Academy of Sciences, China., Hwa Mei Hospital, University of Chinese Academy of Sciences, China; Institute of Life and Health Industry, University of Chinese Academy of Sciences, China. Electronic address: .

Abstract:  An outbreak of Coronavirus Disease 2019 (COVID-19) has spread rapidly. It is imperative to control the epidemic by understanding the epidemiological feature, preventative quarantine, and effective hygiene measures. In the present study, we report a case of super-spreader who transmitted the disease to over twenty-eight persons in Ningbo, Zhejiang. Identifying and isolated super-spreaders, understanding the reasons behind the efficient transmission ability are important for the control and management of the ongoing COVID-19 pandemic. 

Retracted: No

PubPeer comments:
 This paper describes a person who attended a bus tour to a blessing ceremony in a temple. This person appeared to have transferred COVID-19 infection to 25 others during that bus tour. The paper gives a lot of details about this  super-spreader , including their age, place of residence, first letter of their name, marital status and children, and the day that they attended the bus tour. The supplemental material even lists details of the bus tour schedule, which is remarkably uninformative, but worth sharing here: ![file] My question is about whether this patient gave approval to have their details shared in this paper. The paper states *This study was approved by Ethics Committee of our hospital* but in this case, the patient s rights appear to have been forgotten. Could the authors please declare that the patient gave their blessing for this publication? , 
  Given above information, we considered Ms. S as a super-spreader, who can infect 10 or more contacts. Given that this paper is about a  super-spreader , it surprising that there is no discussion about  superspreaders e.g. [1]. [1] https: theconversation.com a-few-superspreaders-transmit-the-majority-of-coronavirus-cases-139950 ,
DNA fastening and ripping actions of novel Knoevenagel condensed dicarboxylic acid complexes in antitumor journey
Authors: Narayanaperumal Pravin
Natarajan Raman
Journal: European Journal of Medicinal Chemistry (2014)
Discipline: CHEMISTRY
Keywords: Antitumor effect; Cytotoxicity; DNA cleavage; Intercalative mode; Oxali-platin type complexes.
Affiliations: Research Department of Chemistry, VHNSN College, Virudhunagar 626 001, Tamil Nadu, India. Electronic address: .

Abstract:  Few novel Cu(II) and Zn(II) oxali-platin type complexes of stoichiometry [ML(ox)] where, L is a Knoevenagel ligand and ox is oxalic acid, have been explored. They are well characterized by spectroanalytical methods. The binding and cleavage propensity of these complexes on DNA and their cytotoxic effect in tumor cells have been investigated. They bind to DNA preferentially by intercalation and cleave the strands under mild reaction conditions even in the absence of external cofactors. However, in H2O2 medium they exhibit better efficacy in the nuclease reaction process by initiating DNA cleavage in an oxidative pattern. Complex 1 shows higher in vitro cytotoxic property against HeLa/EAC cells comparing to other complexes and the standards (cisplatin/5-FU). Moreover, the in vivo antitumor efficacy of copper complexes against EAC tumor model reveals that they are non-toxic to normal cells (lymphocytes). Among the copper complexes, complex 1 reveals excellent antitumor activity. 

Retracted: No

PubPeer comments:
 Could the authors comment on what appear to be some repeated features? ![file] , 
 #1 Fig 6C. ![file] Without these enhancements, 6C is recognisable as a rotated enlarged detail of 6B. ![file] ,
Astragalus injection protects cerebral ischemic injury by inhibiting neuronal apoptosis and the expression of JNK3 after cerebral ischemia reperfusion in rats
Authors: Jinming Song
Guangyi Liu
Zhen Zhou
Tingting Wang
Yunliang Guo
Journal: Behavioral and Brain Functions (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Astragalus; neuroprotective effect; mechanism; cerebral ischemia reperfusion injury; rats
Affiliations: Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong 266003, China. .

Abstract:  Background: Astragalus is a widely used traditional Chinese medicine and has been proven beneficial for many aspects of human health. It is important to explore the neuroprotective effect and mechanism of astragalus injection in cerebral ischemia reperfusion injury. Methods: The focal cerebral ischemic model with middle cerebral artery occlusion (MCAO) reperfusion was established by Longa's method in healthy adult male Wistar rats, and treated by injecting intraperitoneally astragalus injection (3 ml/kg). The neurobehavioral function of rats was evaluated by Longa's test. The cerebral blood flow (CBF) was measured by laser Doppler flowmetry and the cerebral infarct volume was calculated by tetrazolium chloride (TTC) stain. The shape and structure of neurons in parahippocampal area was observed by HE stain and the neuronal apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and flow cytometry. The expressions of c-jun N-terminal kinase 3 (JNK3) mRNA and protein were determined by RT-PCR and immunohistochemical assay and Western blotting respectively. Results: After treatment with astragalus injection, the expressions of JNK3 mRNA and protein reduced significantly, the number of neuronal apoptosis minus, the cerebral infarct volume shrink, the neuronal shape-structure and animal neurobehavioral function improved significantly than those in model rats. Conclusions: It is suggested that astragalus injection could inhibit neuronal apoptosis, reduce infarct volume and improve neurobehavioral function by down-regulating the expression of JNK3 gene after cerebral ischemia reperfusion injury in rats. 

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. ,
Genome-wide incorporation dynamics reveal distinct categories of turnover for the histone variant H3.3
Authors: Wenfei Jin
Daniel C Kraushaar
Misook Ha
Brian Abraham
Alika Maunakea
Keji Zhao
Journal: Genome biology (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Nucleosomes; histone variant H3.3; turnover; genome-wide; mammalian cells

Abstract:  Background: Nucleosomes are present throughout the genome and must be dynamically regulated to accommodate binding of transcription factors and RNA polymerase machineries by various mechanisms. Despite the development of protocols and techniques that have enabled us to map nucleosome occupancy genome-wide, the dynamic properties of nucleosomes remain poorly understood, particularly in mammalian cells. The histone variant H3.3 is incorporated into chromatin independently of DNA replication and requires displacement of existing nucleosomes for its deposition. Here, we measure H3.3 turnover at high resolution in the mammalian genome in order to present a genome-wide characterization of replication-independent H3.3-nucleosome dynamics. Results: We developed a system to study the DNA replication-independent turnover of nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies. Conclusions: We have established a reliable approach to measure turnover rates of H3.3-containing nucleosomes on a genome-wide level in mammalian cells. Our results suggest that distinct mechanisms control the dynamics of H3.3 incorporation at functionally different genomic regions. 

Retracted: No

PubPeer comments:
 February 2016 Erratum, found here: https: genomebiology.biomedcentral.com articles 10.1186 s13059-016-0886-3 It reads:  After the publication of this work [1] an error was noticed in Fig. 1d. In the DAPI columns the same image was used accidentally for the 48 h and 72 h timepoints. The corrected figure is shown below. We apologize for this error. Here is the original Figure 1d, as reported to the journal in July 2015, with red boxes marking the duplicated panels. I thank the authors and journal staff for correcting this error. ![file] ,
Protective effects of memantine against methylmercury-induced glutamate dyshomeostasis and oxidative stress in rat cerebral cortex
Authors: Tianyao Yang
Bin Xu
Yu Deng
Zhaofa Xu
Wei Liu
Yangang Wei
Journal: Neurotoxicity Research (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Methylmercury; neurotoxicity; glutamate; oxidative stress; memantine
Affiliations: Department of Environmental Health, School of Public Health, China Medical University, Shenyang, 110001, Liaoning, People's Republic of China.

Abstract:  Methylmercury (MeHg) is one of the ubiquitous environmental toxicant that leads to long-lasting neurological deficits in animals and humans. The identification of the underlying mechanisms has been a main focus of research in the neurotoxicology field. Glutamate (Glu) dyshomeostasis and oxidative stress have been identified as two critical mechanisms mediating MeHg-induced neurotoxicity. However, little has been known of the interaction between these two mechanisms that play in MeHg poisoning in vivo. We, therefore, developed a rat model of MeHg subchronic poisoning to evaluate its neurotoxic effects and investigated the neuroprotective role of memantine, a low-affinity, noncompetitive N-methyl-D-aspartate receptors (NMDARs) antagonist, against MeHg-induced neurotoxicity. Ninety rats were randomly divided into five groups: control, memantine control, MeHg-treated (4 and 12 μmol/kg), and memantine pretreated. Administration of 12 μmol/kg MeHg for 4 weeks significantly elevated total Hg levels, disrupted Glu metabolism, overexcited NMDARs, and led to intracellular calcium overload, which might be critical to excessive reactive oxygen species (ROS) formation in cerebral cortex. Meanwhile, MeHg administration reduced non-enzymatic (non-protein sulfhydryl, NPSH) and enzymatic (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) antioxidants; caused lipid, protein, and DNA oxidative damage; and enhanced neurocyte apoptosis in cerebral cortex. Moreover, glutamate/aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) appear to be inhibited by MeHg exposure. Pretreatment with memantine at a dose of 5 μmol/kg significantly prevented MeHg-induced alterations of Glu metabolism and oxidative stress, alleviated neurocyte apoptosis, and pathological injury. In conclusion, the results suggested that Glu dyshomeostasis and oxidative stress resulting from MeHg exposure contributed to neuronal injury. Memantine possesses the ability to attenuate MeHg-induced neurotoxicity through mechanisms involving its NMDARs-binding properties and indirect antioxidation. 

Retracted: No

PubPeer comments:
 Figure 12E appears to have a region that has been cut and pasted. Perhaps this was done when relabeling the figure, but it certainly is not a best practice. Could the authors please comment? *** ![file] ,
Synergistic Anti-Tumour Effect of Syk Inhibitor and Olaparib in Squamous Cell Carcinoma: Roles of Syk in EGFR Signalling and PARP1 Activation
Authors: Wei-Yu Chen
Wan-Wan Lin
Chi-Long Chen
Duen-Yi Huang
Nan-Lin Wu
Journal: Cancers (2020)
Discipline: CLINICAL MEDICINE
Keywords: EGFR; PARP; Syk; squamous cell carcinoma.
Affiliations: Department of Pharmacology, College of Medicine, National Taiwan University, Taipei 100, Taiwan., Department of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei 116, Taiwan., Department of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 106, Taiwan., Department of Medicine, Mackay Medical College, New Taipei City 251, Taiwan.

Abstract:  Syk is a non-receptor tyrosine kinase involved in the signalling of immunoreceptors and growth factor receptors. Previously, we reported that Syk mediates epidermal growth factor receptor (EGFR) signalling and plays a negative role in the terminal differentiation of keratinocytes. To understand whether Syk is a potential therapeutic target of cancer cells, we further elucidated the role of Syk in disease progression of squamous cell carcinoma (SCC), which is highly associated with EGFR overactivation, and determined the combined effects of Syk and PARP1 inhibitors on SCC viability. We found that pharmacological inhibition of Syk could attenuate the EGF-induced phosphorylation of EGFR, JNK, p38 MAPK, STAT1, and STAT3 in A431, CAL27 and SAS cells. In addition, EGF could induce a Syk-dependent IL-8 gene and protein expression in SCC. Confocal microscopic data demonstrated the ability of the Syk inhibitor to change the subcellular distribution patterns of EGFR after EGF treatment in A431 and SAS cells. Moreover, according to Kaplan-Meier survival curve analysis, higher Syk expression is correlated with poorer patient survival rate and prognosis. Notably, both Syk and EGFR inhibitors could induce PARP activation, and synergistic cytotoxic actions were observed in SCC cells upon the combined treatment of the PARP1 inhibitor olaparib with Syk or the EGFR inhibitor. Collectively, we reported Syk as an important signalling molecule downstream of EGFR that plays crucial roles in SCC development. Combining Syk and PARP inhibition may represent an alternative therapeutic strategy for treating SCC. 

Retracted: No

PubPeer comments:
 Dear authors, In your discussion section: First paragraph 3rd line,  Nevertheless, long-term EGF treatment also leads to drug resistance, which is an urgent issue that must be overcome . Is this statement valid? Could the authors provide some references? Thank you. ,
Krüppel-like factor 5 mediates proinflammatory cytokine expression in lipopolysaccharide-induced acute lung injury through upregulation of nuclear factor-κB phosphorylation in vitro and in vivo
Authors: Hsiu-Lin Chen
Inn-Wen Chong
Hui-Min Wang
Shyng-Shiou F Yuan
Yi-Chen Lee
Wei-Lun Liu
Po-Len Liu
Jong-Rung Tsai
Journal: Mediators of Inflammation (2014)
Discipline: IMMUNOLOGY
Keywords: Acute lung injury; Krüppel-like factor 5 (KLF5); inflammation; lipopolysaccharide (LPS); proinflammatory cytokine
Affiliations: Department of Respiratory Therapy, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan, Translational Research Center, Department of Medical Research, Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan, Department of Fragrance and Cosmetic Science, Kaohsiung Medical University, Kaohsiung 807, Taiwan, Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan 736, Taiwan

Abstract:  Acute lung injury (ALI) is associated with an inflammation-mediated process, and the transcription factor, Krüppel-like factor 5 (KLF5), might play a crucial role in inflammatory lung disease. In this study, we evaluated KLF5, reactive oxygen species (ROS), and inflammatory responses in a lipopolysaccharide- (LPS-) induced ALI model to elucidate the role of KLF5 in ALI. Our data indicated that LPS upregulates proinflammatory cytokine expression in human bronchial epithelial cells in a dose-dependent manner. We observed upregulated KLF5 protein expression in human bronchial epithelial cells exposed to LPS, with peak expression 1 h after LPS treatment, and subsequent upregulation of p65 protein expression and p65 phosphorylation at Ser276. These results indicate that KLF5 mediates proinflammatory cytokine expression by upregulating nuclear factor-kappaB (NF-κB) phosphorylation at p65 in response to LPS. LPS treatment also increased ROS production and simultaneously upregulated KLF5 expression and NF-κB translocation. N-acetylcysteine significantly reduced ROS levels and KLF5 and NF-κB translocation in nuclear extracts. Therefore, N-acetylcysteine pretreatment before LPS exposure reduces ROS, downregulates KLF5 expression, and subsequently reduces inflammatory responses by scavenging ROS. Overall, our study results indicate that KLF5 mediates proinflammatory cytokine expression through upregulation of NF-κB phosphorylation at p65 in LPS-induced ALI. 

Retracted: No

PubPeer comments:
  Fig.3 TEM images of PtRu MWCNTs (a) and PtRuNi (b) ![file] Here the panels are lined up with their counterparts in Fig. 1 from [Zhao et al (2014)] ,  TEM micrograph of the (a) PtRu(8:2) MWCNTs and (b) PtRuNi(8:1:1) MWCNTs catalysts . ![file] More versions in Fig 1B and 1C of [Zhao et al (2014b)] , where they are  Pt MWCNTs . ![] and in Fig 1 from [Zhao et al (2014c)] where they become Au MWCNTs. ,
Novel Hybrid Gels Made of High and Low Molecular Weight Hyaluronic Acid Induce Proliferation and Reduce Inflammation in an Osteoarthritis In Vitro Model Based on Human Synoviocytes and Chondrocytes
Authors: Annalisa La Gatta
Antonietta Stellavato
Alessio D&#x27;Addona
Mario De Rosa
Anna Virginia Adriana Pirozzi
Giovanni Balato
Valentina Vassallo
Virginia Tirino
Chiara Schiraldi
Carlo Ruosi
Journal: BioMed Research International (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: high molecular weight hyaluronan; HCC; anti-inflammatory effects; rheological behavior; viscosupplement gel
Affiliations: Department of Experimental Medicine, Section of Biotechnology, Medical Histology and Molecular Biology, University of Campania "Luigi Vanvitelli", Naples, Italy., School of Medicine and Surgery "Federico II" of Naples, Department of Public Health, A.O.U. Federico II of Naples, Via S. Pansini, 80131 Naples, Italy., School of Medicine and Surgery “Federico II” of Naples, Department of Public Health, A.O.U. Federico II of Naples, Via S. Pansini, 80131 Naples, Italy

Abstract:  High molecular weight hyaluronan (H-HA) has a pivotal role in the maintenance of normal functions of synovial fluid and structure of the articular joint, but it has been shown that its concentration is reduced in patients affected by degenerative cartilage diseases, such as osteoarthritis (OA). The aim of this study was to investigate the anti-inflammatory effects and properties of hybrid cooperative complexes based on high and low molecular weight hyaluronan (HCC) compared to H-HA on human primary cells derived by pathological joints. In addition, the rheological behavior of HCC was evaluated in order to define their potential as viscosupplement gel in degenerated joints. The experiments were performed using an in vitro model of OA based on human chondrocytes and synoviocytes isolated from degenerated joints of patients hospitalized for surgical replacement. In order to assess the anti-inflammatory effects of HCC, we evaluated NF-kB, COMP-2, IL-6, and IL-8 as specific markers at the transcriptional and/or protein level. Moreover, the proliferative properties of HCC were assessed using time lapse video microscopy. We showed that chondrocytes and synoviocytes clearly presented an altered cytokine profile compatible with a severe ongoing inflammation status. H-HA and, above all, HCC significantly reduced levels of the specific biomarkers evaluated and improved cartilage healing. The rheological profile indicated HCC suitability for intra-articular injection in joint diseases. HCC viscoelastic properties and the protective/anti-inflammatory effect on human chondrocytes and synoviocytes suggest the novel HCC-based gels as a valid support for OA management. 

Retracted: No

PubPeer comments:
 States that  Data Availability Statement: The data presented in this study are available in article and Supplementary Materials but no raw data available, just publicly accessible COI and the summary of some statistics, which is only one element of this study. Can the authors actually provide the raw data? ,
Protective effect of Zhen-Wu-Tang (ZWT) through keeping DA stable and VMAT 2/DAT mRNA in balance in rats with striatal lesions induced by MPTP
Authors: Ji-Min Deng
Chang-Liang Xu
Xiu-Min Li
Lu-Fan Li
Shi-Ping Ma
Rong Qu
Journal: Journal of Ethnopharmacology (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Zhen-Wu-Tang; Parkinson's disease; neuroprotective effect; MPTP; rats
Affiliations: Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, PR China.

Abstract:  Ethnopharmacological relevance: Zhen-Wu-Tang (ZWT), the modified formulation of a classical Chinese prescription from "Treaties on Febrile Disease", was clinically employed to treat Parkinson's disease. Aim of the study: To investigate the neuroprotective effect of ZWT on intra-striatum injection of MPTP-induced Parkinson's disease in rats. Materials and methods: The effect of ZWT on the behavioral changes (open-field test, Ladder walking, spontaneous alternation in Y maze), the dopamine transmitter systems of substantia nigra, striatum and frontal cortex of rats by HPLC-ECD, mRNA expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and vesicular monoamine transporter 2 (VMAT 2) of the above three brain regions was investigated. Results: This study showed that ZWT not only ameliorated the behavior induced by the administration of MPTP in striatum, but also increased DA in the brain, prevented the decreasing of TH and balanced the ratio of VMAT 2/DAT in mRNA level. Conclusions: These results suggest that ZWT possesses neuroprotective and anti-parkinsonism properties. 

Retracted: No

PubPeer comments:
 Figs 7 and 8,  Effect of ZWT on expression of TH, DAT and VMAT 2 mRNA in rat substantia nigra and  Effect of ZWT on expression of TH, DAT and VMAT 2 mRNA in rat striatum . ![file] DAT bands appear to be the same, apart from lightness. ,
Long noncoding RNA NEAT1 promotes nasopharyngeal carcinoma progression through regulation of miR-124/NF-&kappa;B pathway
Authors: Yang Guo
Nan Cheng
Journal: OncoTargets and Therapy (2017)
Discipline: CLINICAL MEDICINE
Keywords: NEAT1; NF-κB pathway; lncRNA; miR-124; nasopharyngeal carcinoma.
Affiliations: Department of Otolaryngology, Huaihe Hospital of Henan University., Department of Ophthalmology, Kaifeng Eye Hospital, Kaifeng Central Hospital, Kaifeng, China.

Abstract:  Nasopharyngeal carcinoma (NPC) is one of the most common malignancies and seriously endangers people's health. Recently, long noncoding RNA (lncRNA) NEAT1 has been determined as an oncogenic gene in a variety of cancers. However, the effect of NEAT1 in NPC and its underlying mechanism have not been well elaborated. In this study, the data showed that NEAT1 was upregulated and miR-124 was downregulated in NPC tissues and cells. Loss-of-function revealed that NEAT1 knockdown inhibited proliferation and promoted apoptosis of NPC cells while gain-of-function revealed that upregulated NEAT1 showed an opposite effect. Moreover, NEAT1 was demonstrated to suppress miR-124 expression by direct interaction in NPC cells. Additionally, miR-124 reversed NEAT1-mediated pro-proliferation and anti-apoptosis effect. Furthermore, miR-124 regulated NPC cell proliferation and apoptosis via NF-κB signal pathway. Mouse models of NPC confirmed that NEAT1 overexpression facilitated tumor growth by modulating miR-124 in vivo. Taken together, this study indicated that upregulated NEAT1 promoted the tumorigenesis and progression of NPC through regulating miR-124/NF-κB signaling pathway, suggesting an attractive therapy target for NPC patients. 

Retracted: No

PubPeer comments:
 In the section Materials Methods, this paper claims to have used a set of PCR primers for NEAT1 in human NP69 cells (Human Nasopharyngeal Epithelial Cell Line). ![file] Following, target analsysis of the primer pair: **Forward: 5u2032-GTACGCGGGCAGACTAACAC-3u2032 Reward: 5u2032- TGCGTCTAGACACCACAACC-3u2032**, it turns out that the combination of these 2 primers is not able to detect any human gene, when using the RNA_Refseq selection in Primer Blast. ![file] **This methodological error renders any claims on quantification of NEAT1 gene expression in all samples unreliable and qualifies for an Expression Of Concern, since many conclusions of this paper are affected, including those modulated by siRNA against NEAT1 (because simply, inhibition can not be confirmed with the primer pair above) .** **Specifically affected are: Fig1A, Fig1B, Fig2A, Fig2B, Fig2C, Fig3A, Fig3B, Fig4B, Fig5E and Table 4**. The authors are welcome to provide raw data and explain these findings above. ,
The mTOR inhibitor AZD8055 inhibits proliferation and glycolysis in cervical cancer cells
Authors: Yan Li
Haifeng Qiu
Shaoru Li
Shijin Wang
Honghua Cai
Weihua Li
Ruili Hu
Journal: Oncology Letters (2013)
Discipline: CLINICAL MEDICINE
Keywords: AZD8055; anticancer activity; cervical cancer; glycolysis; mTOR signaling
Affiliations: Departments of Gynecology and Obstetrics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100;

Abstract:  The aim of the present study was to determine the effect of AZD8055 on proliferation, apoptosis and glycolysis in the human cervical cancer cell line HeLa and to investigate the underlying mechanism(s) of action. HeLa human cervical cancer cells were treated with 10 nM AZD8055 for 24, 48 or 72 h. MTT was used to determine cell proliferation. Annexin V/propidium iodide staining was used to determine cell apoptosis analyzed by fluorescence-activated cell sorting (FACS). Glycolytic activity was determined by measuring the activity of the key enzyme lactate dehydrogenase (LDH) and lactate production. RNA and protein expression were examined by qRT-PCR and western blotting, respectively. Treatment with AZD8055 inhibited proliferation and glycolysis, and induced apoptosis in HeLa cells in a time-dependent manner. During the prolonged treatment with AZD8055, the phosphorylation of mammalian target of rapamycin (mTOR) C1 substrates p70S6K and phosphorylation of the mTORC2 substrate Akt were deregulated, suggesting that the activity of mTOR was downregulated. Furthermore, our study showed that the expression of miR-143 was upregulated in a time-dependent manner in HeLa cells treated with AZD8055. In summary, the present study reveals a novel antitumor mechanism of AZD8055 in HeLa human cervical cancer cells. 

Retracted: No

PubPeer comments:
 Fig 2.  AZD8055 increases apoptosis in cervical cancer cells. Following treatment with 10 nM AZD8055 for 24, 48 and 72 h, HeLa cells were stained with FITC-conjugated Annexin V PI. Percentage of Annexin V PI-stained cells was determined by flow cytometry . ![file] 48- and 72-hour panels are the same. 24-hour panel also appears in Fig 3 of [Xie, Lei Hu (2015)] ,  Cell apoptosis assay was performed in MG63 cells with or without transfection with ECT2u2011specific siRNA . ![file] ,
Phytosynthesis of silver nanoparticles from Jatropha integerrima Jacq. flower extract and their possible applications as antibacterial and antioxidant agent
Authors: Ranganathan Babujanarthanam
Mohamad S AlSalhi
Sandhanasamy Devanesan
Murali Kannan Maruthamuthu
Aruliah Rajasekar
Gunasekaran Suriyakala
Sivaji Sathiyaraj
Journal: Saudi Journal of Biological Sciences (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: E. coli; Jatropha integerrima Jacq.; Silver nanoparticles; Superoxide; X-ray diffraction.
Affiliations: Nano and Energy Bioscience Laboratory, Department of Biotechnology, Thiruvalluvar University, Serkkadu, Vellore 632115, Tamil Nadu, India., Department of Physics and Astronomy, College of Science, King Saud University, P.O. Box - 2455, Riyadh 11451, Saudi Arabia., Environmental Molecular Microbiology Research Laboratory, Department of Biotechnology, Thiruvalluvar University, Serkkadu, Vellore, Tamilnadu 632115, India., Department of Biotechnology & Bioengineering, Purdue University, 610 Purdue Mall, West Lafayette, IN 47907, United States.

Abstract:  Jatropha integerrima Jacq. flower extract was used for the synthesis of silver nanoparticles in the current study. Various spectroscopic analyses were used to characterize the synthesized nanoparticles (JIF-AgNPs). The antibacterial efficacy of JIF-AgNPs was studied by well diffusion and microdilution techniques. In addition, the impact of JIF-AgNPs on free radicals was evaluated. On the ultraviolet-visible spectrum, the nanoparticles exhibit the highest absorbance at 422 nm. Based on the Fourier transform infrared spectrum, phenols and amino acids were involved in capping the JIF-AgNPs. Crystalline sphere-shaped nanoparticles with an average size of 50.07 nm and zeta potential of -19.0 mV were confirmed by X-ray diffraction, transmission electron microscopy, and dynamic light scattering analysis respectively. The JIF-AgNPs exhibit the highest and lowest growth inhibitory activity towards E. coli and B. subtilis. The minimal inhibitory concentration of JIF-AgNPs against E. coli, K. pneumoniae, S. aureus, and B. subtilis were 2.5, 5.0, 5.0, and 7.5 μg/mL, respectively. The JIF-AgNPs exhibited significant radical scavenging activities against DPPH (IC50-32.5 ± 0.06 µg/mL), hydroxyl (IC50-25 ± 0.09 µg/mL), Superoxide (IC50-42.5 ± 0.13 µg/mL), and ABTs (IC50-33.5 ± 0.15 µg/mL). Thus, synthesized nanoparticles were a good alternative to develop an antibacterial and antioxidant agent. 

Retracted: No

PubPeer comments:
null, 
 if the similarities are real, the results of figures 2, 3 and 6 are all distorted , 
null, 
null, 
 https: wol-prod-cdn.literatumonline.com cms attachment 4775fea2-a9dd-49ac-a7b3-1a8b2b55811d jcb25041-fig-0002-m.jpg Recently changed and updated. , 
 A band seems to have been reused for two different conditions in Figure 3f (top) and 5f (bottom). Could the authors please post the original uncropped scans? *** ![file] , 
 Could the authors please compare the images in Figure 4 1b and Figure 4 1f. Is it expected for these to appear so similar? *** ![file] ,
Cerebral mast cells contribute to postoperative cognitive dysfunction by promoting blood brain barrier disruption
Authors: Jie Sun
Susu Zhang
Yanning Qian
Xiang Zhang
Nana Li
Hongquan Dong
Journal: Behavioural Brain Research (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Blood-brain barrier; Cognitive; Mast cell; Neuroinflammation; Postoperative cognitive dysfunction.
Affiliations: Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, PR China., Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, PR China. Electronic address: .

Abstract:  Trauma induced neuroinflammation plays a key role in the development of postoperative cognitive dysfunction (POCD). The blood-brain barrier (BBB), a highly specialized endothelial layer, is exquisitely sensitive to inflammatory insults, which can result in numerous neurocognitive syndromes. While brain mast cells are the "first responder" in the injury, the functional interactions between mast cells and the BBB remain poorly understood. Our results demonstrate that tibial fracture surgery can induce cognitive impairment relating to an inflammatory response and destabilization of the BBB. Disodium cromoglycate (cromolyn)--which acts as a mast cell stabilizer--inhibited this effect. Specifically, cromolyn resulted in ameliorated cognitive ability, decrease of inflammatory cytokines and increase of BBB stability. Taken together, these results suggest that activated mast cells contributed to central nervous system inflammation and cognitive dysfunction by promoting BBB disruption, and interactions between mast cells and the BBB could constitute a new and unique therapeutic target for POCD. 

Retracted: No

PubPeer comments:
 looks like similar than expected, figure 6 ![file] ,
Enhanced susceptibility of oral squamous cell carcinoma cell lines to FAS-mediated apoptosis by cisplatin and 5-fluorouracil
Authors: Masaru Ohashi
Masao Nagumo
Gen Kondo
Hitoshi Watanabe
Masayasu Iwase
Journal: International Journal of Cancer (2003)
Discipline: CLINICAL MEDICINE
Keywords: anticancer drugs; cisplatin; 5-fluorouracil; Fas-mediated apoptosis; oral squamous cell carcinoma
Affiliations: Second Department of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Tokyo, Japan

Abstract:  Our study was conducted to investigate whether anticancer drugs, cisplatin (CDDP) and/or 5-fluorouracil (5-FU), can modulate Fas-mediated apoptosis in oral squamous cell carcinoma (OSCC) cell lines. When OSCC cell lines, NA and HSC-4, were treated with CDDP and/or 5-FU, Fas and its mRNA expression on the plasma membrane were enhanced. An increase in caspase-3 and -8 activities was then observed by the addition of agonistic anti-Fas antibody, CH-11. Apoptosis of OSCC cells treated with anticancer drugs were significantly enhanced by CH-11, whereas untreated cells were nearly resistant to apoptosis. Moreover, the combination of CDDP and 5-FU resulted in an increasing susceptibility to apoptosis. Caspase-3 and -8 inhibitors, but not caspase-9 inhibitor, reduced Fas-mediated apoptosis enhanced by the anticancer drugs. Furthermore, OSCC cells treated with anticancer drugs exhibited decreased cellular FADD-like interleukin 1-converting enzyme-inhibitory protein (c-FLIP) levels, whereas neither the Fas-associated death domain-containing protein (FADD) nor procaspase-8 changed the expression. Moreover, antisense oligonucleotide to c-FLIP confirmed that down-regulation of c-FLIP induced sensitization to Fas-mediated apoptosis. These results suggest that CDDP and 5-FU may enhance the susceptibility to Fas-mediated apoptosis through down-regulation of c-FLIP. From these findings, a new potential strategy may be developed to improve the efficacy of anticancer drugs. 

Retracted: No

PubPeer comments:
 The western blot in Figure 3B has a fairly obvious splicing seam between lanes 2 and 3. Upon enhancing the contrast, it becomes apparent that 2 of the lanes (as indicated here in blue boxes) are cloned. ![file] , 
 2020 retraction. https: www.nature.com articles s41598-020-72330-x The authors have retracted this article. After publication concerns were raised that lanes 1 and 2 and lanes 4 and 5 in Figure 3B appear to be duplications of each other. The authors have confirmed that there are problems with the data presented in this Figure and stated that they no longer have the original data files. All authors agree with this retraction. ,
Curcumin-Mediated Reversal of p15 Gene Promoter Methylation: Implication in Anti-Neoplastic Action against Acute Lymphoid Leukaemia Cell Line
Authors: A Bhatnagar
J Kaur
V Sharma
G Narayan
A K Jha
A Kumar
Journal: Folia biologica (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Curcumin; Anticancer effects; Promoter methylation; p15 gene; Apoptosis
Affiliations: Department of Biotechnology, Panjab University, Chandigarh, India., Department of Biochemistry, Panjab University, Chandigarh, India., Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, India.

Abstract:  Curcumin has been documented to exert anticancer effects by interacting with altered proliferative and apoptotic pathways in cancer models. In this study, we evaluated the potential of curcumin to reverse promoter methylation of the p15 gene in Raji cells and its ability to induce apoptosis and genomic instability. Anti-neoplastic action of curcumin showed an augmentation in reactive oxygen species (ROS) and cell cycle arrest in G1 phase. Subsequently, curcumin- exposed Raji cells showed structural abnormalities in chromosomes. These observations suggest that curcumin also causes ROS-mediated apoptosis and genomic instability. The treatment of Raji cell line with 10 μM curcumin caused hypomethylation of the p15 promoter after six days. Hypomethylation of p15 was further found to be favoured by downregulation of DNA methyltransferase 1 after 10 μM curcumin treatment for six days. Methylation-specific PCR suggested demethylation of the p15 promoter. Demethylation was further validated by DNA sequencing. Reverse-transcription PCR demonstrated that treatment with curcumin (10 μM) for six days led to the up-regulation of p15 and down-regulation of DNA methyltransferase 1. Furthermore, curcumin- mediated reversal of p15 promoter methylation might be potentiated by down-regulation of DNA methyltransferase 1 expression, which was supported by cell cycle analysis. Furthermore, curcumin acts as a double-pronged agent, as it caused apoptosis and promoter hypomethylation in Raji cells. 

Retracted: No

PubPeer comments:
 The authors may want to review the labeling in figures 5A and 6A. Something appears to be incorrect. *** ![file] ,
Non-thermal atmospheric pressure plasma inhibits thyroid papillary cancer cell invasion via cytoskeletal modulation, altered MMP-2/-9/uPA activity
Authors: Seong Jin Seo
Eunpyo Moon
Jae Won Chang
Yoo Seob Shin
Sung Un Kang
Kang Il Kim
Sang Sik Yang
Chul-Ho Kim
Keunho Lee
Jong-Soo Lee
Journal: PloS one (2014)
Discipline: Multidisciplinary
Keywords: Plasma; Non-thermal atmospheric pressure plasma; Cancer research; Invasion; Metastasis
Affiliations: Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Korea., Department of Electrical and Computer Engineering, Ajou University, Suwon, Korea., Department of Molecular Science and Technology and Department of Life Science, Ajou University, Suwon, Korea., Plasma Systems and Materials (PSM) America Inc., Colorado Springs, Colorado, United States of America.

Abstract:  Plasma, the fourth state of matter, is defined as a partially or completely ionized gas that includes a mixture of electrons and ions. Advances in plasma physics have made it possible to use non-thermal atmospheric pressure plasma (NTP) in cancer research. However, previous studies have focused mainly on apoptotic cancer cell death mediated by NTP as a potential cancer therapy. In this study, we investigated the effect of NTP on invasion or metastasis, as well as the mechanism by which plasma induces anti-migration and anti-invasion properties in human thyroid papillary cancer cell lines (BHP10-3 and TPC1). Wound healing, pull-down, and Transwell assays demonstrated that NTP reduced cell migration and invasion. In addition, NTP induced morphological changes and cytoskeletal rearrangements, as detected by scanning electron microscopy and immunocytochemistry. We also examined matrix metalloproteinase (MMP)-2/-9 and urokinase-type plasminogen activator (uPA) activity using gelatin zymography, uPA assays and RT-PCR. FAK, Src, and paxillin expression was detected using Western blot analyses and immunocytochemistry. NTP decreased FAK, Src, and paxillin expression as well as MMP/uPA activity. In conclusion, NTP inhibited the invasion and metastasis of BHP10-3 and TPC1 cells by decreasing MMP-2/-9 and uPA activities and rearranging the cytoskeleton, which is regulated by the FAK/Src complex. These findings suggest novel actions for NTP and may aid in the development of new therapeutic strategies for locally invasive and metastatic cancers. 

Retracted: No

PubPeer comments:
 Several issues have been reported to the journal in 2015. Figure 2C. * Yellow boxes. In the TPC-1 row, the Control and Gas panels appear to show an overlap. ![file] , 
 Figure 3. * Red boxes: In the GTP-Cdc42 panels, lane 4 of the left panel looks similar to lane 1 of the right panel. ![file] , 
 Figure 7B. * Pink boxes. The two 18S panels, which represent different cells, appear to look very similar. ![file] , 
 Figure S5. * Green boxes: Two panels appear to show an overlap. ![file] ,
SARS-CoV-2 detection in patients with influenza-like illness
Authors: Leyi Wang
Ming-Wei Peng
Yao Li
Xiao-Bing Yang
Wen-Hua Kong
De-Guang Kong
Man-Qing Liu
Journal: Nature microbiology (2020)
Discipline: MICROBIOLOGY
Keywords: COVID-19; SARS-CoV-2; Wuhan; community transmission; throat swabs
Affiliations: Wuhan Center for Disease Control & Prevention, Wuhan, Hubei, China., Department of Veterinary Clinical Medicine, Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Illinois, Urbana, IL, USA., Wuhan Center for Disease Control & Prevention, Wuhan, Hubei, China. .

Abstract:  Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first reported in Wuhan, Hubei Province, China in late December 2019. We re-analysed 640 throat swabs collected from patients in Wuhan with influenza-like-illness from 6 October 2019 to 21 January 2020 and found that 9 of the 640 throat swabs were positive for SARS-CoV-2 RNA by quantitative PCR, suggesting community transmission of SARS-CoV2 in Wuhan in early January 2020. 

Retracted: No

PubPeer comments:
 u201cWe performed a commercial quantitative PCR assay (BioGerm) approved by the China CDC and National Medical Products Administration to detect the presence of SARS-CoV-2 in the throat swab specimens of patients with ILI. The targets of this assay were both the ORF1ab and N gene of SARS-CoV-2, and the detection limit was 1,000 copies mlu22121.u201d Two queries about the methodology: 1) What is the product code of the BioGerm PCR assay? 2) which primers probes in supplementary table 1 correspond to the detection of u201cboth the ORF1ab and N gene of SARS-CoV-2u201d? , 
 #1 1) The product code of BioGerm PCR assay for SARS-CoV-2 is ZC-HX-201-2; 2) The primers listed in Supplementary table 1 was for the detection and subtyping of influenza virus, not for SARS-CoV-2. ,
miR-663b promotes colorectal cancer progression by activating Ras/Raf signaling through downregulation of TNK1
Authors: Sen Hong
Helei Wang
Zhenkun Yan
Lei Ding
Miaomiao Bi
Yumei Song
Journal: Human Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Colorectal cancer; TNK1; microR-663b.
Affiliations: Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun, 130021, Jilin, People's Republic of China., Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun, 130022, Jilin, People's Republic of China., Department of Gastrointestinal Surgery, The First Hospital of Jilin University, Changchun, 130021, Jilin, People's Republic of China. ., Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun, 130022, Jilin, People's Republic of China. ., Department of Thoracic Oncology, Tumor Hospital of Jilin Province, Changchun, Jilin, People's Republic of China., Department of Ophthalmology, The China-Japan Union Hospital of Jilin University, Jilin University, Changchun, 130022, Jilin, People's Republic of China.

Abstract:  MiR-663b has been demonstrated to be abnormally expressed in several cancer types and was involved in the progression of cancer. Although overexpression of miR-663b in colorectal cancer was observed, the role of miR-663b in colorectal cancer cells has not been identified yet. In this study, we analyzed expression of miR-663b in colorectal tumors and explored the molecular mechanism of miR-663b in colorectal cancer cells. MiR-663b was significantly overexpressed in colorectal tumors and cell lines. Downregulation of miR-663b inhibited cell proliferation and sphere forming ability in colorectal cancer cells. In addition, miR-663b downregulation inactivated Ras/Raf signaling activity and subsequently decreased YAP1 and CD44 expression in colorectal cancer cells. Using TargetScan software, TNK1, a negative regulator of Ras/Raf signaling, was predicted to be a target gene of miR-663b. Western blotting and RT-qPCR showed that TNK1 expression was negatively regulated by miR-663b. In addition, the direct binding of miR-663b to TNK1 mRNA was proved by dual luciferase reporter assay. Furthermore, downregulation of miR-663b inhibited colorectal cancer cell proliferation and stemness, which was reversed after siRNA-mediated silencing of TNK1. In conclusion, the current study revealed a pivotal role of miR-663b in the progression of colorectal cancer. 

Retracted: No

PubPeer comments:
 Some of the bands in Figure 3C appear similar. Could the authors please share uncropped original scans? *** Inverse ![file] *** Original ![file] ,