PReD-Bench/PRed-Bench huggingface dataset:
Molecular Diagnosis of a Novel Coronavirus (2019-nCoV) Causing an Outbreak of Pneumonia
Authors: Daisy Y M Ng
Samuel M S Cheng
Pavithra Krishnan
Kenrie P Y Hui
Yingzhi Liu
Leo L M Poon
Peng Yang
Malik Peiris
Quanyi Wang
Daniel K W Chu
Yang Pan
Carrie K C Wan
Journal: Clinical Chemistry (2020)
Discipline: CLINICAL MEDICINE
Keywords: novel coronavirus; 2019-nCoV; real-time reverse-transcription PCR assays; SARS coronavirus; human-to-human transmission
Affiliations: School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, Beijing Center for Disease Prevention and Control, Beijing, China, Beijing Research Center for Preventive Medicine, Beijing, China, School of Public Health, Capital Medical University, Beijing, China

Abstract:  Background: A novel coronavirus of zoonotic origin (2019-nCoV) has recently been identified in patients with acute respiratory disease. This virus is genetically similar to SARS coronavirus and bat SARS-like coronaviruses. The outbreak was initially detected in Wuhan, a major city of China, but has subsequently been detected in other provinces of China. Travel-associated cases have also been reported in a few other countries. Outbreaks in health care workers indicate human-to-human transmission. Molecular tests for rapid detection of this virus are urgently needed for early identification of infected patients. Methods: We developed two 1-step quantitative real-time reverse-transcription PCR assays to detect two different regions (ORF1b and N) of the viral genome. The primer and probe sets were designed to react with this novel coronavirus and its closely related viruses, such as SARS coronavirus. These assays were evaluated using a panel of positive and negative controls. In addition, respiratory specimens from two 2019-nCoV-infected patients were tested. Results: Using RNA extracted from cells infected by SARS coronavirus as a positive control, these assays were shown to have a dynamic range of at least seven orders of magnitude (2x10-4-2000 TCID50/reaction). Using DNA plasmids as positive standards, the detection limits of these assays were found to be below 10 copies per reaction. All negative control samples were negative in the assays. Samples from two 2019-nCoV-infected patients were positive in the tests. Conclusions: The established assays can achieve a rapid detection of 2019n-CoV in human samples, thereby allowing early identification of patients. 

Retracted: No

PubPeer comments:
 These tests are all getting non-specific results - this may lead to unnecessary quarantining of ppl. As in other tests - the like [the CDC] - [this test will get SARS] . There is a [great 500bp] for specific testing of Wuhan coronavirus. ,
p73beta-Mediated apoptosis requires p57kip2 induction and IEX-1 inhibition
Authors: Susana Gonzalez
Eva Hernando
Carlos Cordon-Cardo
Manuel M Perez-Perez
Manuel Serrano
Journal: Cancer Research (2005)
Discipline: CLINICAL MEDICINE
Keywords: p73alpha; p73beta; apoptosis; DNA damage; caspase activation
Affiliations: Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 

Abstract:  Similarly to p53, p73alpha and p73beta induce growth arrest and/or apoptosis in response to DNA damage or when exogenously expressed. However, how they trigger apoptosis remains unresolved. After stable transduction of either p73alpha or p73beta, a greater apoptotic response was observed for p73beta in both primary and tumor cells. Consistently, blocking ectopic and endogenous p73beta expression by specific shRNA significantly decreased apoptotic levels after DNA damage. We found that p73beta targets the apoptotic program at multiple levels: (i) facilitating caspase activation through p53-dependent signals and (ii) inducing p57KIP2, while down-regulating c-IPA1 and IEX1 through a p53-independent mechanism. p73beta-mediated apoptosis was considerably reduced after inhibition of p57(KIP2) by small interfering RNA, IEX-1 overexpression, and in mouse embryo fibroblasts derived from p57-/- mice. Data from this study offer evidence for the apoptotic activity exclusive of p73beta. In the clinical context, these results might have potential therapeutic implications, because p73beta could induce alternative apoptotic responses in tumors harboring p53 mutations. 

Retracted: No

PubPeer comments:
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 Figure 3B. Much more similar than expected after horizontal flip. ![file] ,
A novel micro-linear vector for in vitro and in vivo gene delivery and its application for EBV positive tumors
Authors: Ge Zhang
Shou-Yi Chen
Chris K C Wong
John P Giesy
Hong-Sheng Wang
Xue-Ling Ou
Zhuo-Jia Chen
Jun Du
Xiang-Ling Yang
Journal: PLoS ONE (2012)
Discipline: Multidisciplinary
Keywords: gene delivery vector; Micro-Linear vector (MiLV); transfection efficiency; safety; clinical application
Affiliations: Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, People's Republic of China. 

Abstract:  Background: The gene delivery vector for DNA-based therapy should ensure its transfection efficiency and safety for clinical application. The Micro-Linear vector (MiLV) was developed to improve the limitations of traditional vectors such as viral vectors and plasmids. Methods: The MiLV which contained only the gene expression cassette was amplified by polymerase chain reaction (PCR). Its cytotoxicity, transfection efficiency in vitro and in vivo, duration of expression, pro-inflammatory responses and potential application for Epstein-Barr virus (EBV) positive tumors were evaluated. Results: Transfection efficiency for exogenous genes transferred by MiLV was at least comparable with or even greater than their corresponding plasmids in eukaryotic cell lines. MiLV elevated the expression and prolonged the duration of genes in vitro and in vivo when compared with that of the plasmid. The in vivo pro-inflammatory response of MiLV group was lower than that of the plasmid group. The MEKK1 gene transferred by MiLV significantly elevated the sensitivity of B95-8 cells and transplanted tumor to the treatment of Ganciclovir (GCV) and sodium butyrate (NaB). Conclusions: The present study provides a safer, more efficient and stable MiLV gene delivery vector than plasmid. These advantages encourage further development and the preferential use of this novel vector type for clinical gene therapy studies. 

Retracted: No

PubPeer comments:
 Figure four appears to have a number of overlapping images. Shown below with enhanced brightness. *** ![file] *** Original ![file] ,
Enhanced Luminescent Properties of Photo-Stable Copper Nanoclusters through Formation of “Protein-Corona”-Like Assemblies
Authors: Saptarshi Mukherjee
Subhajit Chakraborty
Madhumita Mukherjee
Nirmal Kumar Das
Journal: ChemPhysChem (2018)
Discipline: CHEMISTRY
Keywords: Luminescence; nano-bio assemblies; nanoclusters; photo-stable; protein-corona.
Affiliations: Department of Chemistry; Indian Institute of Science Education and Research Bhopal; Bhopal Bypass Road, Bhauri, Bhopal 426 066 Madhya Pradesh India, Department of Chemistry, Indian Institute of Science Education and Research Bhopal, Bhopal Bypass Road, Bhauri, Bhopal, 426 066, Madhya Pradesh, India.

Abstract:  In this study, interactions of synthesized copper nanoclusters (CuNCs) with a model transport protein, human serum albumin (HSA), have been systematically investigated by using various spectroscopic approaches. The interactions give rise to the formation of "protein-corona" like assemblies and the luminescence properties (both steady-state and time-resolved) are enhanced due to gradual adsorption of the protein on the surface of the NCs. The associated thermodynamics and binding parameters have been estimated resorting to luminescent experimental techniques as well as isothermal titration calorimetry (ITC) studies, indicating that every NC is surrounded by (4±1) protein molecules. The adsorption of HSA on the surface of the NCs has been characterized by dynamic light scattering (DLS) and time-resolved anisotropy measurements. Finally, fluorescence correlation spectroscopy (FCS) data substantiate the emergence of new "protein-corona" like assemblies resulting in slower translational diffusion motions and concomitant rise of the hydrodynamic diameters. 

Retracted: No

PubPeer comments:
 There is some confusion regardin the enhancement of fl. intenisty of CuNCs on addition of HSA. The enhancement of fluorescence intenisty of CuNCs upon addition of HSA at around 450 nm is probably due to the HSA itself as explained in  Direct Evidence of Intrinsic Blue Fluorescence from Oligomeric Interfaces of Human Serum Albumin by Mukherjee et al. Have the authors carried out this fl. study uisng only the HSA at the same concentration ( that is without CuNCs)? It doesn t seem so, because a 500 micromol HSA has high fluorescence intensity as depicted by Mukherjee et el in the same region. ,
Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation
Authors: Hans-Uwe Simon
Sally Hopkins-Donaldson
Larisa L Belyanskaya
Stefanie Kurtz
Rolf Stahel
Shida Yousefi
Uwe Zangemeister-Wittke
Ana Paula Simões-Wüst
Journal: International Journal of Cancer (2005)
Discipline: CLINICAL MEDICINE
Keywords: survivin; small cell lung cancer; PI3K/Akt pathway; cisplatin; apoptosis
Affiliations: Laboratory of Molecular Oncology, Department of Oncology, University Hospital Zurich, Zurich, Switzerland.

Abstract:  The inhibitor of apoptosis protein (IAP) survivin is overexpressed in many tumors but is absent in most normal adult tissues. We report high levels of survivin expression in small cell lung cancer (SCLC), and describe the role of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in survivin upregulation. Moreover, the cytoprotective function of survivin in response to the anti-cancer agent cisplatin (CDDP) was investigated. Negative modulation of PI3K/Akt using pharmacological inhibitors or dominant negative Akt (DN-Akt) decreased Akt kinase activity and resulted in decreased survivin expression and phosphorylation on Thr34, whereas transfection of constitutively active Akt (CA-Akt) increased survivin expression and phosphorylation. Interestingly, we found that treatment of SCLC cells with CDDP further increased survivin expression in a cell cycle independent manner by activation of Akt. CA-Akt or lentiviral survivin also inhibited apoptosis induced by CDDP, whereas DN-Akt or survivin-specific RNA interference sensitized cells to CDDP. We identified survivin as an anti-apoptotic protein in SCLC cells that is regulated by Akt, and demonstrate that treatment with the DNA damaging agent CDDP activates the PI3K/Akt/survivin pathway that in part protects cells from drug-induced apoptosis. 

Retracted: No

PubPeer comments:
 Figure 2D. Splices in some panels, but not in others. ![file] ,
Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis
Authors: Wenjing Qin
Huiping Li
Fangfang Liu
Journal: Cancer Cell International (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CBLL1; DDP; NSCLC; circ_0072083; miR-545-3p.
Affiliations: Department of Respiratory Medicine, First Affiliated Hospital of Henan University, No. 357, Ximen Street, Longting District, Kaifeng, 475000 Henan China.

Abstract:  Background: Non-small-cell lung cancer (NSCLC) is one of the common cancers in the world. Circular RNA 0072083 (circ_0072083, circZFR) has been reported to be associated with the progression of NSCLC. In this study, we intended to explore the role and the potential mechanism of circ_0072083 in NSCLC. Methods: Quantitative real time polymerase chain reaction (qRT-PCR) was performed to detect the expression of circ_0072083, its matching linear RNA (zinc finger RNA binding protein (ZFR)) and microRNA-545-3p (miR-545-3p) in NSCLC cells. The ability of colony formation in NSCLC cells was detected by colony formation assay. The apoptosis and cell cycle were measured by flow cytometry. The metastasis was determined by transwell migration and invasion assays. The protein expression of E-cadherin, N-cadherin, Vimentin and Cbl proto-oncogene like 1 (CBLL1) was examined by western blot assay. The interaction between miR-545-3p and circ_0072083 or CBLL1 was predicted by starBase or Targetscan software. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to validate these interactions. Nude mice bearing tumors were used to confirm the role of circ_0072083 and cisplatin (DDP) in vivo. Results: The level of circ_0072083 was higher in NSCLC tissues and cells relative to that in adjacent non-tumor tissues and normal lung cells. The transfection of si-circ_0072083 inhibited colony formation, cell cycle and metastasis while promoted the apoptosis of NSCLC cells stimulated by DDP. MiR-545-3p was a direct functional target of circ_0072083 in NSCLC cells. CBLL1 could bind to miR-545-3p in NSCLC cells. Circ_0072083 promoted the progression of NSCLC induced by DDP through sponging miR-545-3p and enhancing the enrichment of CBLL1 in vivo and in vitro. Conclusion: Circ_0072083 depletion contributed to DDP-triggered inhibition of NSCLC tumor through miR-545-3p/CBLL1 axis. 

Retracted: No

PubPeer comments:
 Figure 2 appears to have an image duplication. ![file] ,
Mammalian target of rapamycin up-regulation of pyruvate kinase isoenzyme type M2 is critical for aerobic glycolysis and tumor growth
Authors: June Goto
Youyong Lu
Jianhui Ma
Han You
Yanling Jing
Xinxin Chen
Tong Chen
Hiroaki Onda
Qian Sun
Ming-Rong Wang
Xiaojun Zha
Rongrong Chen
Hongwang Yang
David Kwiatkowski
Yanan Wang
Haiyong Peng
Fang Wang
Long Chang
Hongbing Zhang
Yu Zhang
Journal: Proceedings of the National Academy of Sciences of the United States of America (2011)
Discipline: Multidisciplinary
Keywords: aerobic glycolysis; Warburg effect; cancer cells; glycolytic enzyme; pyruvate kinase M2 (PKM2)
Affiliations: State Key Laboratory of Medical Molecular Biology, Department of Physiology and Pathophysiology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100005, China.

Abstract:  Although aerobic glycolysis (the Warburg effect) is a hallmark of cancer, key questions, including when, how, and why cancer cells become highly glycolytic, remain less clear. For a largely unknown regulatory mechanism, a rate-limiting glycolytic enzyme pyruvate kinase M2 (PKM2) isoform is exclusively expressed in embryonic, proliferating, and tumor cells, and plays an essential role in tumor metabolism and growth. Because the receptor tyrosine kinase/PI3K/AKT/mammalian target of rapamycin (RTK/PI3K/AKT/mTOR) signaling cascade is a frequently altered pathway in cancer, we explored its potential role in cancer metabolism. We identified mTOR as a central activator of the Warburg effect by inducing PKM2 and other glycolytic enzymes under normoxic conditions. PKM2 level was augmented in mouse kidney tumors due to deficiency of tuberous sclerosis complex 2 and consequent mTOR activation, and was reduced in human cancer cells by mTOR suppression. mTOR up-regulation of PKM2 expression was through hypoxia-inducible factor 1α (HIF1α)-mediated transcription activation, and c-Myc-heterogeneous nuclear ribonucleoproteins (hnRNPs)-dependent regulation of PKM2 gene splicing. Disruption of PKM2 suppressed oncogenic mTOR-mediated tumorigenesis. Unlike normal cells, mTOR hyperactive cells were more sensitive to inhibition of mTOR or glycolysis. Dual suppression of mTOR and glycolysis synergistically blunted the proliferation and tumor development of mTOR hyperactive cells. Even though aerobic glycolysis is not required for breach of senescence for immortalization and transformation, the frequently deregulated mTOR signaling during multistep oncogenic processes could contribute to the development of the Warburg effect in many cancers. Components of the mTOR/HIF1α/Myc-hnRNPs/PKM2 glycolysis signaling network could be targeted for the treatment of cancer caused by an aberrant RTK/PI3K/AKT/mTOR signaling pathway. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,
Formulation, optimization, hemocompatibility and pharmacokinetic evaluation of PLGA nanoparticles containing paclitaxel
Authors: Gunjan Vasant Bonde
Ramit Kapoor
Brahmeshwar Mishra
Pooja Mittal
Harsh Vardhan
Ashu Mittal
Gufran Ajmal
Journal: Drug development and industrial pharmacy (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Box–Behnken design; Nanoparticles; hemocompatibility; optimization; paclitaxel
Affiliations: Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (IIT) BHU, Varanasi, India;, Amity Institute of Pharmacy, Amity University, Noida, India;, Canberra Institute of Technology (CIT), Canberra (ACT), Australia

Abstract:  Objective: Paclitaxel (PTX)-loaded polymer (Poly(lactic-co-glycolic acid), PLGA)-based nanoformulation was developed with the objective of formulating cremophor EL-free nanoformulation intended for intravenous use. Significance: The polymeric PTX nanoparticles free from the cremophor EL will help in eliminating the shortcomings of the existing delivery system as cremophor EL causes serious allergic reactions to the subjects after intravenous use. Methods and results: Paclitaxel-loaded nanoparticles were formulated by nanoprecipitation method. The diminutive nanoparticles (143.2 nm) with uniform size throughout (polydispersity index, 0.115) and high entrapment efficiency (95.34%) were obtained by employing the Box-Behnken design for the optimization of the formulation with the aid of desirability approach-based numerical optimization technique. Optimized levels for each factor viz. polymer concentration (X1), amount of organic solvent (X2), and surfactant concentration (X3) were 0.23%, 5 ml %, and 1.13%, respectively. The results of the hemocompatibility studies confirmed the safety of PLGA-based nanoparticles for intravenous administration. Pharmacokinetic evaluations confirmed the longer retention of PTX in systemic circulation. Conclusion: In a nutshell, the developed polymeric nanoparticle formulation of PTX precludes the inadequacy of existing PTX formulation and can be considered as superior alternative carrier system of the same. 

Retracted: No

PubPeer comments:
 Fig 12 has image duplication as shown. Interesting artifacts shown within yellow circles. Similar artifact could be seen in panel D. I would leave it to authors and readers to notice an additional artifact common in panels F-H. Could authors post unedited source files for all panels shown in this figure? ![file] ,
Advances in the treatment options for vitiligo: activated low-dose cytokines-based therapy
Authors: Giuseppe Fabrizi
Torello Lotti
Jana Hercogova
Journal: Expert opinion on pharmacotherapy (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: IL-1; IL-10; IL-4; TNF-α; anti-IL-1 antibodies
Affiliations: a 1 University of Rome "G.Marconi" , Rome, Italy ., b 2 Dermatology Clinic Bulovka - Dermatology Bulovka Hospital , Prague Czech Republic., c 3 University of Parma - Clinica Dermatologica , Parma, Italy.

Abstract:  Introduction: Vitiligo is a skin disorder characterized by a progressive depigmentation, which is caused by the loss of melanocytes at the cutaneous level. A shift of the immune system with a prevalence of T helper (Th)1/Th17 response instead of a Tregs/Th2 one and may be part of etiology of 10 vitiligo. Areas covered: This review describes the major points of vitiligo onset and shows the cutting-edge results in the field of low-dose medicine in the treatment of dermatologic diseases and, in particular. in vitiligo. In this review on advances in vitiligo pharmacotherapy, the most pertinent recent publications are reported. Electronic databases such as PubMed were searched for terms 'low-dose medicine' or 'low dose and vitiligo' or 'low dose and psoriasis.' Expert opinion: The availability of a systemic treatment for vitiligo, based on the oral administration of low-dose activated signaling molecules represents an opportunity for the dermatologists to overcome some specific pitfalls of currently available therapeutic protocols. 

Retracted: No

PubPeer comments:
 The titular  Expert Opinion here appears to be an advertisement for the homeopathic preparations sold by GUNA, of Milan. The company s main departure from the methods of classical homeopathy was to replace the term  succussion with  SKA , for Sequential Kinetic Activation. Both terms describe the stage of striking the preparation during the process of sequential dilution, imparting the properties of the original medicinal molecules to the dilutant solvent, even as those original molecules are diluted out of existence. * Low doses of activated cytokines, antibodies, neuropeptides, hormones and growth factors are orally administered in order to restore the biological balance of a pathologically altered cellular cross-talk in accordance with P.N.E.I. principles. An innovative pharmaceutical activation technology called sequential kinetics activation (SKA); a pharmaceutical productive technique (codified and standardized by GUNA Laboratories -- Italy) allows the nano-concentrations (in the range of pg ml and fg ml) to be active even below the classically considered minimum pharmacologically effective concentration [21]. * I cannot find the word  homeopathy used anywhere in the paper. This seems a little disingenuous. Anyway, do Taylor Francis really want to be associated with a form of medical malpractice centered on placebos? I am puzzled that this piece was ever published. The [board of editors] does include Uwe Wollina, frequent Lotti co-author and [not a stranger to PubPeer] , but this may not be relevant. ,
Sensitization strategies in lung cancer
Authors: Peiying Zhang
Xiao-Ying Zhang
Journal: Oncology Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: cancer; resistance; sensitization approaches; tumor.
Affiliations: Nanjing University of Chinese Medicine, Information Institute, Nanjing, Jiangsu 210029, P.R. China., Department of Cardiology, Xuzhou Central Hospital, The Affiliated Xuzhou Hospital of Medical College of Southeast University, Xuzhou, Jiangsu 221009, P.R. China.

Abstract:  The commonly used treatment avenues employed by cancer physicians include surgery, radiotherapy (RT) and chemotherapy in addition to rapid developmental and confirmatory studies on the efficacy of targeted therapies. However, the success rate in these commonly used treatments remains relatively low due to associated side effects, such as normal cell targeting/toxicity and resistance. In addition, investigators are continuing their efforts to enhance the efficacy of RT and chemotherapy to prevent associated side effects and improve the survival rate of the affected patient in order to increase patient survival. In the present study, we have reviewed the sensitization approaches used to improve chemotherapy and RT sensitivity in tumors. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader. This 2016 review paper appears to be unexpectedly similar to a 2015 PhD thesis by Katarzyna Zielinska-Chomej at the Karolinska Institutet, Sweden, called  Analysis and characterization of chemo- and radiation therapy sensitizing strategies in tumours with focus on effects of phenothiazines on DNA damage response signalling . That 2015 thesis can be found here: https: openarchive.ki.se xmlui bitstream handle 10616 44651 Thesis_Katarzyna_Zielinska-Chomej.pdf?sequence=1 isAllowed=y Of note, several other review papers by Zhang and Zhang published in Oncology Letters have been retracted for plagiarism of other PhD theses. See DOIs 10.3892 ol.2016.5093, 10.3892 ol.2016.5107, 10.3892 ol.2016.5134, 10.3892 ol.2016.5200, 10.3892 ol.2016.5242, 10.3892 ol.2016.5260, 10.3892 ol.2016.5302, and 10.3892 ol.2016.5322. Here is a marked-up version of the text by Zhang and Zhang 2016, with highlighted text showing similarities to the thesis. Generated in SimTexter . On the left is the original 2015 text by Zielinska-Chomej, on the right the Zhang and Zhang 2016 review. ![file] Two close-up views in higher resolution: ![file] ![file] ,
LPS unmasking of Shigella flexneri reveals preferential localisation of tagged outer membrane protease IcsP to septa and new poles
Authors: Elizabeth Ngoc Hoa Tran
Renato Morona
Matthew Thomas Doyle
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Shigella flexneri; outer membrane protease; IcsP; Omptin family; IcsA
Affiliations: Discipline of Microbiology and Immunology, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, Australia.

Abstract:  The Shigella flexneri outer membrane (OM) protease IcsP (SopA) is a member of the enterobacterial Omptin family of proteases which cleaves the polarly localised OM protein IcsA that is essential for Shigella virulence. Unlike IcsA however, the specific localisation of IcsP on the cell surface is unknown. To determine the distribution of IcsP, a haemagglutinin (HA) epitope was inserted into the non-essential IcsP OM loop 5 using Splicing by Overlap Extension (SOE) PCR, and IcsP(HA) was characterised. Quantum Dot (QD) immunofluorescence (IF) surface labelling of IcsP(HA) was then undertaken. Quantitative fluorescence analysis of S. flexneri 2a 2457T treated with and without tunicaymcin to deplete lipopolysaccharide (LPS) O antigen (Oag) showed that IcsP(HA) was asymmetrically distributed on the surface of septating and non-septating cells, and that this distribution was masked by LPS Oag in untreated cells. Double QD IF labelling of IcsP(HA) and IcsA showed that IcsP(HA) preferentially localised to the new pole of non-septating cells and to the septum of septating cells. The localisation of IcsP(HA) in a rough LPS S. flexneri 2457T strain (with no Oag) was also investigated and a similar distribution of IcsP(HA) was observed. Complementation of the rough LPS strain with rmlD resulted in restored LPS Oag chain expression and loss of IcsP(HA) detection, providing further support for LPS Oag masking of surface proteins. Our data presents for the first time the distribution for the Omptin OM protease IcsP, relative to IcsA, and the effect of LPS Oag masking on its detection. 

Retracted: No

PubPeer comments:
 This editor-in-chief has been involved in over 100 publications in his own journal-Indoor and Built Environment. After I have been reported this issue in a Chinese social media and now we can only get over 30 publication records from SAGE s Indoor and Built Environment page: https: journals.sagepub.com action doSearch?target=default ContribAuthorStored=Yu%2C+Chuck+Wah Nevertheless, we could still find his publication records on his own Journal from SAGE, see below link: https: journals.sagepub.com action doSearch?filterOption=allJournal AllField=Chuck+yu It has been widely recognized that Editor-in-chiefs should always avoid publishing too many articles in the journals he she own, but this editor-in-chief, is an exception. ,
Presynaptic glycine receptors increase GABAergic neurotransmission in rat periaqueductal gray neurons
Authors: Michiko Nakamura
Kwi-Hyung Choi
Il-Sung Jang
Journal: Neural Plasticity (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: periaqueductal gray; nociceptive transmission; glycine receptors; glutamatergic transmission; EPSCs
Affiliations: Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea.

Abstract:  The periaqueductal gray (PAG) is involved in the central regulation of nociceptive transmission by affecting the descending inhibitory pathway. In the present study, we have addressed the functional role of presynaptic glycine receptors in spontaneous glutamatergic transmission. Spontaneous EPSCs (sEPSCs) were recorded in mechanically dissociated rat PAG neurons using a conventional whole-cell patch recording technique under voltage-clamp conditions. The application of glycine (100 µM) significantly increased the frequency of sEPSCs, without affecting the amplitude of sEPSCs. The glycine-induced increase in sEPSC frequency was blocked by 1 µM strychnine, a specific glycine receptor antagonist. The results suggest that glycine acts on presynaptic glycine receptors to increase the probability of glutamate release from excitatory nerve terminals. The glycine-induced increase in sEPSC frequency completely disappeared either in the presence of tetrodotoxin or Cd(2+), voltage-gated Na(+), or Ca(2+) channel blockers, suggesting that the activation of presynaptic glycine receptors might depolarize excitatory nerve terminals. The present results suggest that presynaptic glycine receptors can regulate the excitability of PAG neurons by enhancing glutamatergic transmission and therefore play an important role in the regulation of various physiological functions mediated by the PAG. 

Retracted: No

PubPeer comments:
 Title does not match the contents of the paper: The title claims a change in GABAergic currents, but the paper is about glutamatergic inputs. The authors use dissociated cells, but still they find synaptic inputs? I would be interested to know how that works..... , 
 Maybe synapses are still attached to the dissociated cells? Activating a chloride conductance could also depolarise those presynaptic terminals, because chloride concentrations can be elevated in axons? , 
 #1 There was a mistake in the title of this paper. We will contact with the Journal Office to fix this mistake. ,
Hesperetin Induces the Apoptosis of Gastric Cancer Cells via Activating Mitochondrial Pathway by Increasing Reactive Oxygen Species
Authors: Jixiang Zhang
Vikash
Dandan Wu
Jia Song
Jiasheng Yi
Weiguo Dong
Jing Wang
Journal: Digestive Diseases and Sciences (2015)
Discipline: CLINICAL MEDICINE
Keywords: Apoptosis; Gastric cancer; Hesperetin; Mitochondria; Reactive oxygen species.
Affiliations: Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, China. ., Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, China.

Abstract:  Background: Hesperetin, has been shown to exert biological activities on various types of human cancers. However, few related studies on gastric cancer are available. Aim: In this study, we sought to investigate the effect of hesperetin on gastric cancer and clarify its specific mechanism. Materials and methods: Cell Counting Kit-8, 2',7'-dichlorofluorescin diacetate, JC-1, Hoechst 33258 staining, and western bolt were used to detect cell viability, levels of intracellular reactive oxygen species (ROS), changes in mitochondrial membrane potential (△ψ m), cell apoptosis, and expressions of mitochondrial pathway proteins, respectively. Meanwhile, xenograft tumor models in nude mice were made to evaluate the effect of hesperetin on gastric cancer in vivo. Results: Compared with the control group, the proliferation of gastric cancer cells in hesperetin groups was significantly inhibited (P &lt; 0.05), and dose- and time-dependent effects were observed. Pretreatment with H2O2 (1 mM) or N-acetyl-L-cysteine (5 mM) enhanced or attenuated the hesperetin-induced inhibition of cell viability (P &lt; 0.05). Percentages of apoptotic cells, levels of intracellular ROS, and △ψ m varied with the dose and treatment time of hesperetin (P &lt; 0.05), and hesperetin caused an increase in the levels of AIF, Apaf-1, Cyt C, caspase-3, caspase-9, and Bax and a decrease in Bcl-2 levels (P &lt; 0.05). Meanwhile, hesperetin significantly inhibited the growth of xenograft tumors (P &lt; 0.05). Conclusion: Our study suggests that hesperetin could inhibit the proliferation and induce the apoptosis of gastric cancer cells via activating the mitochondrial pathway by increasing the ROS. 

Retracted: No

PubPeer comments:
 In Figure 5A, it looks like one of the Western blots has 10 lanes (WCL; anti-HA), whereas the corresponding blots have 9 lanes. I expect that the first lane in the HA blot to be blank due to the low MW of HA (1.1 kDa)? I am also wondering why the strong HA staining for KLF2 and KLF4 is presented at a much higher MW than the other proteins. They should have the approx similar MW. Furthermore, KLF2 and KLF have different MW. ![file] ,
CSN6 promotes malignant progression of oral squamous cell carcinoma by down-regulating TIMP-2
Authors: J Wang
W-Y Gao
J-M He
P Wang
G Yang
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: CSN6; oral squamous cell carcinoma; TIMP-2; malignant progression; metastasis
Affiliations: Oral Clinical Medicine Centre, Gansu Provincial Hospital, Lanzhou, Gansu, China. .

Abstract:  Objective: This study was designed to investigate the expression characteristics of CSN6 in oral squamous cell carcinoma (OSCC), and to further explore the mechanism of how it promotes the malignant progression of this cancer. Patients and methods: The expressions of CSN6 and TIMP-2 in tumor tissue samples and adjacent normal ones collected from 36 OSCC patients were detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the interplay between their expression levels and the clinical indicators or prognosis of OSCC patients was analyzed as well. Meanwhile, the expressions of CSN6 and TIMP-2 in OSCC cell lines were further verified via qRT-PCR. In addition, CSN6 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines, CAL-27, and Tca8113. At the same time, transwell and cell wound healing assays were conducted to uncover the impact of CSN6 on the function of OSCC cells. Finally, the potential mechanism was explored using Luciferase reporter gene and recovery experiments. Results: In this work, qRT-PCR results revealed that the level of CSN6 in tumor tissues of OSCC patients was remarkably higher than that in adjacent normal ones. Compared with patients with low expression of CSN6, those with high expression CSN6 had a higher incidence of lymph node or distant metastasis and a lower overall survival rate. In vitro experiments revealed that silencing CSN6 remarkably attenuated the invasive, as well as migration capacities of OSCC cells while overexpression of CSN6 conversely enhanced those. Subsequently, in OSCC cell lines and tissues, TIMP-2 expression was remarkably reduced, which was negatively correlated with CSN6 level. Bioinformatics and Luciferase reporter genes demonstrated that CSN6 can target the corresponding sites of TIMP-2 promoter. In addition, cell recovery experiments suggested the existence of a mutual regulation between CSN6 and TIMP-2, which may synergistically modulate the malignant progression of OSCC. Conclusions: The above results indicated that CSN6 was remarkably upregulated both in OSCC tissues and cell lines, which is remarkably relevant to the incidence of lymph node or distant metastasis and poor prognosis of OSCC patients. Additionally, we verified that CSN6 may promote OSCC malignant progression by regulating TIMP-2. 

Retracted: No

PubPeer comments:
 If this is published in Scientific Programming, it certainly should be related to Scientific Programming. But I struggle to understand the relation. --- Academic Editor: Qinhu Zhang (Currently listed as a regular paper, was previously a part of a special issue.) ,
TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions
Authors: Daehwan Kim
Harold Pimentel
Geo Pertea
Cole Trapnell
Ryan Kelley
Steven L Salzberg
Journal: Genome biology (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TopHat2; spliced aligner; RNA-sequence; RNA-seq; indels

Abstract:  TopHat is a popular spliced aligner for RNA-sequence (RNA-seq) experiments. In this paper, we describe TopHat2, which incorporates many significant enhancements to TopHat. TopHat2 can align reads of various lengths produced by the latest sequencing technologies, while allowing for variable-length indels with respect to the reference genome. In addition to de novo spliced alignment, TopHat2 can align reads across fusion breaks, which can occur after genomic translocations. TopHat2 combines the ability to identify novel splice sites with direct mapping to known transcripts, producing sensitive and accurate alignments, even for highly repetitive genomes or in the presence of pseudogenes. TopHat2 is available at http://ccb.jhu.edu/software/tophat. 

Retracted: No

PubPeer comments:
 Readers should become aware of a preprint entitled  Comment on u201cTopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusionsu201d by Kim et al. that re-examine TopHat2 analyses perfomerd in Kim et al., 2013 paper. https: www.biorxiv.org content 10.1101 000851v1 From the Abstract:  In the recent paper [1] (thereafter referred to as u201cTopHat2paperu201d) the accuracy of TopHat2 was compared to other RNA-seq aligners. In this comment we re-examine most important analyses from the TopHat2paper and identify several deficiencies that significantly diminished performance of some of the aligners, including incorrect choice of mapping parameters, unfair comparison metrics, and unrealistic simulated data. Using STAR [2] as an exemplar, we demonstrate that correcting these deficiencies makes its accuracy equal or better than that of TopHat2. Furthermore, this exercise highlighted some serious issues with the TopHat2 algorithms, such as poor recall of alignments with a moderate ( 3) number of mismatches, low sensitivity and high false discovery rate for splice junction detection, loss of precision for the realignment algorithm, and large number of false chimeric alignments. ,
Retracted: A Study of Potential SARS-CoV-2 Antiviral Drugs and Preliminary Research of Their Molecular Mechanism, Based on Anti-SARS-CoV Drug Screening and Molecular Dynamics Simulation
Authors: Zhi Miao
Wenyu Lu
Xiaomeng Zhao
Nan Ye
Ruixia Liu
Journal: Journal of Computational Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 2019-nCoV; COVID-19; SARS-CoV-2; molecular docking; remdesivir.
Affiliations: School of Chemical Engineering and Technology, Tianjin University, Tianjin, P.R. China., Tianjin Cosmo Biotechnology Co. Ltd., Tianjin, P.R. China., Key Laboratory of System Bioengineering (Tianjin University), Ministry of Education, Tianjin, P.R. China., Collaborative Innovation Center of Chemical Science and Engineering (Tianjin), SynBio Res Platform, Tianjin, P.R. China.

Abstract:  At the request of the corresponding author, Dr. Wenyu Lu, of the published article entitled "A Study of Potential SARS-CoV-2 Antiviral Drugs and Preliminary Research of Their Molecular Mechanism, Based on Anti-SARS-CoV Drug Screening and Molecular Dynamics Simulation" by Xiaomeng Zhao, Ruixia Liu, Zhi Miao, Nan Ye, and Wenyu Lu (J Comput Biol; epub 1 Dec 2020; https://doi.org/10.1089/cmb.2020.0112), Journal of Computational Biology officially retracts the paper. Dr. Lu stated in his communication to the Editor that, "due to personal reasons, our data is not perfect enough. I want to modify and add some content; I want to withdraw the manuscript." Though Dr. Lu did not provide details of the specific problems with the data, the Editor and Publisher agreed to the request to retract the paper. 

Retracted: Yes

PubPeer comments:
 Retracted on 25 June, 2021: https: www.liebertpub.com doi 10.1089 cmb.2020.0112.retract  At the request of the corresponding author, Dr. Wenyu Lu, of the published article entitled, u201cA Study of Potential SARS-CoV-2 Antiviral Drugs and Preliminary Research of Their Molecular Mechanism, Based on Anti-SARS-CoV Drug Screening and Molecular Dynamics Simulationu201d by Xiaomeng Zhao, Ruixia Liu, Zhi Miao, Nan Ye, and Wenyu Lu (J Comput Biol; epub 1 Dec 2020; https: doi.org 10.1089 cmb.2020.0112), Journal of Computational Biology officially retracts the paper. Dr. Lu stated in his communication to the Editor that, u201cdue to personal reasons, our data is not perfect enough. I want to modify and add some content; I want to withdraw the manuscript.u201d Though Dr. Lu did not provide details of the specific problems with the data, the Editor and Publisher agreed to the request to retract the paper. ,
Enhanced combination therapy effect on paclitaxel-resistant carcinoma by chloroquine co-delivery via liposomes
Authors: Yuzhen Xu
Menghua Gao
Liyan Qiu
Journal: International Journal of Nanomedicine (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: chloroquine; combination therapy; drug resistance; liposome; paclitaxel.
Affiliations: College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, People's Republic of China., Ministry of Education (MOE) Key Laboratory of Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, People's Republic of China ; Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu, People's Republic of China.

Abstract:  A novel composite liposomal system co-encapsulating paclitaxel (PTX) with chloroquine phosphate (CQ) was designed for treating PTX-resistant carcinoma. It was confirmed that liposomal CQ can sensitize PTX by means of autophagy inhibition and competitively binding with multidrug-resistance transporters. Furthermore, according to the in vitro cytotoxicity and apoptosis assay, real-time observation of cellular uptake, and in vivo tissue distribution study, co-encapsulation of PTX and CQ in liposomes was validated as superior to the mixture of PTX liposome plus CQ liposome due to the simultaneous delivery and synergetic effect of the two drugs. Consequently, this composite liposome achieved significantly stronger anticancer efficacy in vivo than the PTX liposome plus CQ liposome mixture. This study helps to guide and enlighten ongoing and future clinical trials about the optimal administration modes for drug combination therapy. 

Retracted: No

PubPeer comments:
 Figure 6A appears to have been touched up. This may be due to relabeling, but it certainly is not a best practice. *** ![file] ,
Effects of Panax Notoginseng Saponins on Homing of C-kit+ Bone Mesenchymal Stem Cells to the Infarction Heart in Rats
Authors: Qing-Yong He
Jin-Sheng Zhang
Tao Huang
Bao-Xia Zhang
Journal: Journal of Traditional Chinese Medicine (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Panax notoginseng saponins; C-kit+ bone mesenchymal stem cells; homing; acute myocardial infarction; G-CSF

Abstract:  Objective: To investigate the effects of panax notoginseng saponins (PNS) on homing of C-kit+ bone mesenchymal stem cells (BMSCs) to the infarction heart. Methods: The acute myocardial infraction (AMI) model was established in 140 Wistar rats, 105 model rats survived after operation, and the model rats were randomly divided into five groups, 21 rats in each group: Western medicine group mobilized by subcutaneous injection of human granuloctye colony stimulating factor (G-CSF) 50 microg x kg(-1) x d(-1); sham operation group and a model group treated by subcutaneous injection of normal saline 50 microg x kg(-1) x d(-1); Chinese medicine group mobilized by intraperitoneal injection of Xuesaitong (see text) (ingredients of PNS) 150 mg x kg(-1) x d(-1); integrative medicine group mobilized by subcutaneous injection of G-CSF 50 microg x kg(-1) x d(-1) and intraperitoneal injection of Xuesaitong 150 mg x kg(-1) x d(-1). Except for the sham-operated group, each group was divided into three sub-groups by three time points of 1 d, 7 d and 14 d. G-CSF was injected once a day for 7 d. Xuesaitong was injected once a day until the rats were killed. The flow cytometry was used for detection of C-kit+ cells in the peripheral blood in different time points, and immunohistochemical method was used for detection of the changes of C-kit+ cell and Ki-67+ cell numbers in the marginal zone of AMI. Results: Twenty-four hours after the operation, C-kit+ cells had a slight increase in the model group compared with the sham operation group (P &gt; 0.05). The peripheral blood C-kit+ cells in the integrative group increased significantly compared with the other groups on 7 d and 14 d (all P &lt; 0.05). Meanwhile the expression of C-kit+ cells and Ki-67+ cells in the marginal zone of AMI in the integrative group increased significantly compared with the Chinese medicine group, the western medicine group and the model group on 1 d, 7 d and 14 d (all P &lt; 0.05), and the cells in the integrative group decreased significantly on 14 d compared with that on 7 d (P &lt; 0.05). Conclusion: PNS can cooperate with G-CSF to mobilize C-kit+ BMSCs from the marrow into the peripheral blood and promote them "homing" to the infarction heart. 

Retracted: No

PubPeer comments:
 Figures 6 and 10 appear to share a common origin. I did not check elsewhere in the paper. *** Contrast enhanced ![file] ,
Mechanism of As2O3 induces apoptosis of glioma U87 cells
Authors: G-B Wang
J-H Liu
J Hu
K Xue
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: arsenic trioxide; apoptosis; glioma cells; proliferation; p53
Affiliations: Department of Neurosurgery, Yantaishan Hospital, Yantai, China. .

Abstract:  Objective: To investigate the mechanism of arsenic trioxide (As2O3)-induced apoptosis of glioma cells. Materials and methods: U87 cells were treated by different concentrations of As2O3 (8 μmol/L, 6 μmol/L, 4 μmol/L, 2 μmol/L, 1 μmol/L and 0.5 μmol/L) for 24 h, 48 h and 72 h, respectively. Cell viability was detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the appropriate dosage and time were screened. Transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was used to stain cells, followed by an investigation on the apoptosis of cells. In the study of molecular mechanism, the expression of p53 in the cells was determined by immunofluorescence, and then apoptosis-related factors, Fas, FasL and Bax, were tested using Real-time polymerase chain reaction (RT-PCR). Finally, the effect of As2O3 on apoptosis-related proteins, caspase-3 and caspase-9, was investigated by Western blotting. Results: As2O3 could significantly inhibit proliferation of U87 cells, and the result of TUNEL staining displayed As2O3 had the function of inducing apoptosis. Immunofluorescence results demonstrated that p53 was highly expressed in glioma cells, which was reduced after drug administration. The results of detection of apoptosis factors using RT-PCR revealed that mRNA expressions of Fas, FasL and Bax in the glioma cells were distinctly higher than those in the As2O3 group. The result of Western blotting indicated that caspase-3 and caspase-9 proteins were highly expressed in glioma cells. Analysis of variance showed that the difference between the control group and the As2O3 group was statistically significant (p&lt;0.01). Conclusions: As2O3 can inhibit proliferation of glioma cells and induce its apoptosis, which may be correlated with down-regulation of expressions of apoptosis-related factors, Fas, FasL and Bax, and apoptosis-related proteins, p53, caspase-3 and caspase-9. 

Retracted: No

PubPeer comments:
 Figure 2.  TUNEL staining results of Control group and As2O3 treatment group. ![file] Please compare with Figure 4 from [Geng et al (2018)] .  TUNEL staining results of antagonism of CST against CsA-induced apoptosis of H9C2 cells . ![] I speculate that the present  As2O3-8 panel was the original for  CsA , that  As2O3-6 (horizontally flipped) became  CsA+CST 0.025 , that  As2O3-4 (rotated and flipped) became  CsA+CST 0.1 and  CsA+CST 0.05 ,