PReD-Bench/PRed-Bench huggingface dataset:
M(3) muscarinic receptor antagonist bencycloquidium bromide attenuates allergic airway inflammation, hyperresponsiveness and remodeling in mice
Authors: Meng-Jing Bao
Yi-Cheng Xie
Qiang-Min Xie
Yang-Mei Deng
Jun-Xia Jiang
Fen-Fen Li
Xin-Wei Dong
Rui Cao
Xiao-Feng Yan
Jun-Shan He
Xiao-Ping Chen
Journal: European Journal of Pharmacology (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: M(3) muscarinic receptors; bencycloquidium bromide; airway hyperresponsiveness; inflammation; airway remodeling
Affiliations: Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Medical College of Zhejiang University, Hangzhou, China.

Abstract:  M(3) muscarinic receptors are localized on inflammatory cells, airway smooth muscle, and submucosal glands, known to mediate bronchoconstriction, mucus secretion, and airway remodeling. It is hypothesized bencycloquidium bromide (BCQB), a novel M(3) receptor antagonist, might have potential effects on airway hyperresponsiveness, inflammation and airway remodeling in a murine model of asthma. Mice sensitized and challenged with ovalbumin developed airway inflammation. Bronchoalveolar lavage fluid was examined to determine the total and differential cell counts, and cytokine levels. Lung tissues were evaluated for cell infiltration, mucus hypersecretion, airway remodeling, and the expression of inflammatory biomarkers. Airway hyperresponsiveness was monitored by direct airway resistance analysis. Inhalation administration of BCQB significantly not only reduced ovalbumin-induced airway hyperresponsiveness comparing to methacholine, and prevented the ovalbumin-induced increase in total cell counts and eosinophil counts. Reverse transcriptase polymerase chain reaction analysis of whole lung lysates revealed that BCQB markedly suppressed ovalbumin-induced mRNA expression of eotaxin, IL-5, IL-4 and MMP-9, and increased mRNA expression of IFN-γ and TIMP-1 in a dose-dependent manner. Substantial IFN-γ/IL-4 (Th1/Th2) levels were recovered in bronchoalveolar lavage fluid after BCQB treatment. In addition, histological studies showed that BCQB dramatically inhibited ovalbumin-induced lung tissue eosinophil infiltration, airway mucus production and collagen deposition in lung tissues. Results reported in current paper suggest that M(3) receptors antagonist may provide a novel therapeutic approach to treat airway inflammation, hyperresponsiveness and remodeling. 

Retracted: No

PubPeer comments:
 Fig 3 A,C.  Ginsenoside shortens the cell cycle of MG-63 and Saos-2 cells. A: flow chart of MG-63 cell cycle in response to the treatment of different concentration of ginsenoside... C: flow chart of Saos-2 cell cycle in response to the treatment of different concentration of ginsenoside . Unexpected overhangs in these graphs. What equipment was used to plot them? ![file] ,
Heterogeneous integration of rigid, soft, and liquid materials for self-healable, recyclable, and reconfigurable wearable electronics
Authors: Zhanan Zou
Pengcheng Zhu
Wei Zhang
Chuanqian Shi
Jianliang Xiao
Zepeng Lei
Journal: Science Advances (2020)
Discipline: Multidisciplinary
Keywords: Wearable electronics; monitoring; physical activities; health conditions; human-computer interfaces
Affiliations: School of Aerospace Engineering and Applied Mechanics, Tongji University, Shanghai 200092, China., Department of Mechanical Engineering, University of Colorado, Boulder, Boulder, CO 80309, USA., Department of Chemistry, University of Colorado Boulder, Boulder, CO 80309, USA.

Abstract:  Wearable electronics can be integrated with the human body for monitoring physical activities and health conditions, for human-computer interfaces, and for virtual/augmented reality. We here report a multifunctional wearable electronic system that combines advances in materials, chemistry, and mechanics to enable superior stretchability, self-healability, recyclability, and reconfigurability. This electronic system heterogeneously integrates rigid, soft, and liquid materials through a low-cost fabrication method. The properties reported in this wearable electronic system can find applications in many areas, including health care, robotics, and prosthetics, and can benefit the well-being, economy, and sustainability of our society. 

Retracted: No

PubPeer comments:
 I am concerned that the bottom two panels in figure (3E) appears to contain a single ECG recording which has been time-shifted to be represented as two ECGs taken in separate conditions. ![file] The structure of high-frequency noise in an ECG does not permit this to be real - it is stochastic, and in reality does not contain regularities like this. Can the authors clarify? ,
Up-regulation of GABA transporters and GABA(A) receptor α1 subunit in tremor rat hippocampus
Authors: Jiqun Cai
Zhanyou Wang
Tianbao Chen
Chris Shaw
Feng Guo
Ni Xie
Dongyu Min
Junling Yu
Xiaoyuan Mao
Journal: Neuroscience Letters (2010)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: GABAergic neurotransmission; epileptogenesis; GABA transporters; GABA receptors; tremor rat
Affiliations: Department of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang 110001, China.

Abstract:  The loss of GABAergic neurotransmission has been closely linked with epileptogenesis. The modulation of the synaptic activity occurs both via the removal of GABA from the synaptic cleft and by GABA transporters (GATs) and by modulation of GABA receptors. The tremor rat (TRM; tm/tm) is the parent strain of the spontaneously epileptic rat (SER; zi/zi, tm/tm), which exhibits absence-like seizure after 8 weeks of age. However, there are no reports that can elucidate the effects of GATs and GABA(A) receptors (GABARs) on TRMs. The present study was conducted to detect GATs and GABAR α1 subunit in TRMs hippocampus at mRNA and protein levels. In this study, total synaptosomal GABA content was significantly decreased in TRMs hippocampus compared with control Wistar rats by high performance liquid chromatography (HPLC); mRNA and protein expressions of GAT-1, GAT-3 and GABAR α1 subunit were all significantly increased in TRMs hippocampus by real time PCR and Western blot, respectively; GAT-1 and GABAR α1 subunit proteins were localized widely in TRMs and control rats hippocampus including CA1, CA3 and dentate gyrus (DG) regions whereas only a wide distribution of GAT-3 was observed in CA1 region by immunohistochemistry. These data demonstrate that excessive expressions of GAT-1 as well as GAT-3 and GABAR α1 subunit in TRMs hippocampus may provide the potential therapeutic targets for genetic epilepsy. 

Retracted: No

PubPeer comments:
 Figure S5A showed identical image for WT and KO, could the authors please show the raw data and explain? ![file] , 
 #1 This is unfortunately an unintended mistake, and we are working with the journal to correct it. The conclusion still stands the same. -Xiaohu Wang and Chen Dong ,
Role of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi's sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma
Authors: Ethel Cesarman
Amy Chadburn
Daniel M Knowles
Shannon Keller
Daniel L Di Bartolo
Ilaria Guasparri
Hongyu Deng
Ren Sun
Elizabeth Hyjek
Journal: Journal of Virology (2009)
Discipline: MICROBIOLOGY
Keywords: Primary effusion lymphoma; PEL; Kaposi's sarcoma-associated herpesvirus; KSHV; human herpesvirus 8
Affiliations: Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065, USA.

Abstract:  Primary effusion lymphoma (PEL) is a distinct type of B-cell non-Hodgkin lymphoma characterized by the presence of Kaposi's sarcoma-associated herpesvirus (KSHV/human herpesvirus 8). Despite having a genotype and gene expression signature of highly differentiated B cells, PEL does not usually express surface or cytoplasmic immunoglobulin (Ig). We show the lack of Oct-2 and OCA-B transcription factors to be responsible, at least in part, for this defect in Ig production. Like Ig genes, ORF50, the key regulator of the switch from latency to lytic reactivation, contains an octamer motif within its promoter. We therefore examined the impact of Oct-2 and OCA-B on ORF50 activation. The binding of Oct-1 to the ORF50 promoter has been shown to significantly enhance ORF50 transactivation. We found that Oct-2, on the other hand, inhibited ORF50 expression and consequently lytic reactivation by competing with Oct-1 for the octamer motif in the ORF50 promoter. Our data suggest that Oct-2 downregulation in infected cells would be favorable to KSHV in allowing for efficient viral reactivation. 

Retracted: No

PubPeer comments:
null, 
 #1 Cell lines are different, yet the IgVH and actin PCR products look very similar. , 
 ![file] ,
Methylglyoxal Induces Changes in the Glyoxalase System and Impairs Glutamate Uptake Activity in Primary Astrocytes
Authors: Franciane Lirio
Fernanda Hansen
Daniela Fraga de Souza
André Quincozes-Santos
Carollina Da Ré
Rafaela Ferreira Pacheco
Adriana Fernanda Vizuete
Fabiana Galland
Marina Concli Leite
Carlos-Alberto Gonçalves
Journal: Oxidative Medicine and Cellular Longevity (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: astrocyte functions; diabetes mellitus; neurodegenerative diseases; methylglyoxal; glyoxalase 1 activity
Affiliations: Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, 90035-003 Porto Alegre, RS, Brazil, Universidade Feevale, Rio Grande do Sul, 93525-075 Novo Hamburgo, RS, Brazil

Abstract:  The impairment of astrocyte functions is associated with diabetes mellitus and other neurodegenerative diseases. Astrocytes have been proposed to be essential cells for neuroprotection against elevated levels of methylglyoxal (MG), a highly reactive aldehyde derived from the glycolytic pathway. MG exposure impairs primary astrocyte viability, as evaluated by different assays, and these cells respond to MG elevation by increasing glyoxalase 1 activity and glutathione levels, which improve cell viability and survival. However, C6 glioma cells have shown strong signs of resistance against MG, without significant changes in the glyoxalase system. Results for aminoguanidine coincubation support the idea that MG toxicity is mediated by glycation. We found a significant decrease in glutamate uptake by astrocytes, without changes in the expression of the major transporters. Carbenoxolone, a nonspecific inhibitor of gap junctions, prevented the cytotoxicity induced by MG in astrocyte cultures. Thus, our data reinforce the idea that astrocyte viability depends on gap junctions and that the impairment induced by MG involves glutamate excitotoxicity. The astrocyte susceptibility to MG emphasizes the importance of this compound in neurodegenerative diseases, where the neuronal damage induced by MG may be aggravated by the commitment of the cells charged with MG clearance. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A34 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
miR-346 functions as a pro-survival factor under ER stress by activating mitophagy
Authors: Junfei Guo
Hua Tang
Zhen Yang
Min Liu
Tong Li
Xi Yang
Journal: Cancer Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: Autophagy; ER stress; GSK3B; UPR; miR-346.
Affiliations: Tianjin Life Science Research Center, Department of Pathogen, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China; Department of Clinical Laboratory of Guangdong Women and Children Hospital, Guangzhou, China., Tianjin Life Science Research Center, Department of Pathogen, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China., Tianjin Life Science Research Center, Department of Pathogen, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. Electronic address: .

Abstract:  Stress in the endoplasmic reticulum (ER) triggers the unfolded protein response (UPR), which attempts to restore normal function of the ER. Both autophagy and miRNAs have been reported to participate in the process of ER stress, but the relationship between these two factors is still obscure. In this study, we demonstrated that miR-346, which was induced under ER stress, modulated autophagic flux in HeLa cells. By regulating the process of autophagy, miR-346 reduced the ROS level in the cells, thus protecting them from death following ER stress. Furthermore, we demonstrated that GSK3B was the target of miR-346 and participated in ER stress-related autophagy. miR-346 activated autophagy by interrupting the association between BCL2 and BECN1 in a GSK3B-dependent manner. Our findings shed new light on the role of miRNAs during ER stress and suggest a new mechanism for the induction of autophagy under ER stress. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have a repeated image. *** ![file] , 
 Correction, August 15, 2020: https: www.sciencedirect.com science article pii S0304383520303724?via%3Dihub  The authors regret that two panels (Fig. 3 A pcDNA3+TG Fig. 3E shR-BECN1+ pri-miR-346 Tg) in Fig. 3 in article entitled u201cmiR-346 functions as a pro-survival factor under ER stress by activating mitophagyu201d Cancer Lett. 2018 01 28;413,69u201381 are wrongly placed by mistake. They checked their original data and found that the panel of Fig. 3 A pcDNA3 Tg was inadvertently duplicated in the panel Fig. 3E shR-BECN1+ pri-miR-346 Tg during the process of preparing Fig. 3, and they did not notice the error due to their careless. They wish to correct the mistake and the conclusion of the paper did not change by the correction. The corrected Fig. 3 is given below. ,
Gulf War syndrome as a part of the autoimmune (autoinflammatory) syndrome induced by adjuvant (ASIA)
Authors: E Israeli
Journal: Lupus (2012)
Discipline: CLINICAL MEDICINE
Keywords: Gulf War syndrome; multi-symptom condition; signs and symptoms; muscle fatigue; tiredness
Affiliations: The Zabludowicz Center for Autoimmune Diseases, Chaim Sheba Medical Center, Tel-Hashomer, Israel. 

Abstract:  Gulf War syndrome (GWS) is a multi-symptom condition comprising a variety of signs and symptoms described in the literature, which not been fully resolved. The various symptoms of the condition include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. In addition, excessive chemical sensitivity and odour intolerance is reported. The aetiology of the condition is unclear, but many reviews and epidemiological analyses suggest association with pyridostigmine bromide (PB), certain vaccination regimes, a variety of possible chemical exposures, including smoke from oil-well fires or depleted uranium from shells, as well as physical and psychological stress. Recently, Shoenfeld et al. suggested that four conditions--siliconosis, macrophagic myofaciitis (MMF), GWS and post-vaccination phenomena--that share clinical and pathogenic resemblances, may be incorporated into common syndrome called 'Autoimmune (Autoinflammatory) Syndrome induced by Adjuvants' (ASIA). Symptoms and signs of the four conditions described by Shoenfeld et al. show that at least eight out of ten main symptoms are in correlation in all four conditions. Namely, myalgia, arthralgias, chronic fatigue, neurological cognitive impairment, gastrointestinal symptoms, respiratory symptoms, skin manifestations and appearance of autoantibodies. Regardless of the aetiology of GWS, be it exposure to environmental factors or chemical drugs, vaccinations or the adjuvants in them, GWS fits well with the definition of ASIA and is included as part of 'Shoenfeld's syndrome'. 

Retracted: No

PubPeer comments:
 https: twitter.com PracheeAC status 1347929009699643395 https: twitter.com PappulabWashU status 1347955910359060481 ,
Downregulated microRNA‐224 aggravates vulnerable atherosclerotic plaques and vascular remodeling in acute coronary syndrome through activation of the TGF‐β/Smad pathway
Authors: Mei-Hua Sun
Gong-Liang Guo
Hai-Ming Xu
Feng-Hua Sui
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TGF-β/Smad pathway; acute coronary syndrome; microRNA-224; vascular remodeling; vulnerable atherosclerotic plaque.
Affiliations: Department of CardiologyChina‐Japan Union Hospital of Jilin UniversityChangchun China, Department of PediatricsThe First Hospital of Jilin UniversityChangchun China

Abstract:  Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR-224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF-β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR-224 inhibitor was prepared for investigating the effect of downregulated miR-224 on the contents of nitric oxide (NO) and endothelin-1 (ET-1), blood lipid levels and inflammatory factor levels in serum as well as the TGF-β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high-density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET-1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM-1 and MMP-2 protein expression, TGF-β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF-β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR-224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF-β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS. 

Retracted: Yes

PubPeer comments:
  FIGURE 3 Reduced miRu2010224 expression or activated TGFu2010u03b2 Smad pathway deteriorated histopathological changes of the thoracic aorta of MI rats detected by HE staining . NC and miR-224 Inhibitor images probably come from the same aorta, since they overlap. ![file] , 
 Retracted [13 April 2022] . ------------------------ The above article, published online on 14 October 2018 in Wiley Online Library , has been retracted by agreement between the authors, the journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed after the authors asked for correction and following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. The editors consider the conclusions of this article to be invalid. ,
Down-regulated microRNA-183 mediates the Jak/Stat signaling pathway to attenuate hippocampal neuron injury in epilepsy rats by targeting Foxp1
Authors: Xianbing Cheng
Mingqiong Yuan
Xidong Chen
Wei Xiong
Xiankun Zhu
Zhijie Wei
Xiangyong Feng
Jian Zhan
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Foxp1; Jak/Stat signaling pathway; MicroRNA-183.
Affiliations: Department of Rehabilitation Medicine, Affiliated hospital of zunyi medical university , Zunyi , Guizhou , PR. China., Department of Neurology, The Second Affiliated Hospital of Zunyi Medical University , Zunyi , Guizhou , PR. China., Department of Neurology, Affiliated hospital of zunyi medical university , Zunyi , Guizhou , PR. China.

Abstract:  Recently, the impacts of microRNAs (miRNAs) have been identified in epilepsy (EP), this study was designed to assess the role of miR-183 in hippocampal neuron injury in EP. Rat EP models were established by injected with lithium-pilocarpine. The pathological observation of rats' hippocampus sections was conducted. Expression of miR-183, Foxp1, Jak1, Stat1, and Stat3 in rats' hippocampal tissues was determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. The proliferation ability and the apoptosis of the rats' neurons were measured. Furthermore, the target relation between miR-183 and Foxp1 was determined by bioinformatics analysis and dual-luciferase gene reporter assay. The levels of miR-183, Jak1, Stat1, and Stat3 were elevated, and the expression of Foxp1 was declined in EP rats' hippocampal tissues. Inhibited miR-183 could up-regulate Foxp1, inhibited miR-183 together with up-regulated Foxp1 could repress hippocampal neuron injury, promote neuron proliferation, suppress neuron apoptosis, and inactivate the Jak/Stat signaling pathway, resulting in an attenuation of EP progression. Moreover, down-regulated Foxp1 could reverse the attenuation of EP progression which was contributed by inhibited miR-183. Our study implies that inhibited miR-183 could up-regulate Foxp1, resulting in an inactivation of the Jak/Stat signaling pathway and promotion of neuron proliferation, as well as inhibition of apoptosis of hippocampal neurons in EP rats, by which the hippocampal neuron injury and EP progression could be repressed. 

Retracted: No

PubPeer comments:
 ![file] ![file] ![file] , 
 #1 Fig 2B. Pink boxes indicate two panels that are surprisingly similar (after a 90-deg flip). Orange ovals are roughly the area where the panels differ. Blue boxes indicate two panels with surprising similarities (after a vertical flip). ![file] ,
Modulation of the vitamin D3 response by cancer-associated mutant p53
Authors: Ira Kogan
Moshe Oren
Perry Stambolsky
Revital Maor-Aloni
Lilach Weisz
Moshe Shay
Itamar Simon
Eyal Kalo
Yuval Tabach
Idit Shiff
Varda Rotter
Giulia Fontemaggi
Zehava Siegfried
Giovanni Blandino
Journal: Cancer Cell (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p53 gene; mutp53 protein; ChIP-on-chip analysis; vitamin D receptor (VDR); gain-of-function mechanism
Affiliations: Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel. 

Abstract:  The p53 gene is mutated in many human tumors. Cells of such tumors often contain abundant mutant p53 (mutp53) protein, which may contribute actively to tumor progression via a gain-of-function mechanism. We applied ChIP-on-chip analysis and identified the vitamin D receptor (VDR) response element as overrepresented in promoter sequences bound by mutp53. We report that mutp53 can interact functionally and physically with VDR. Mutp53 is recruited to VDR-regulated genes and modulates their expression, augmenting the transactivation of some genes and relieving the repression of others. Furthermore, mutp53 increases the nuclear accumulation of VDR. Importantly, mutp53 converts vitamin D into an antiapoptotic agent. Thus, p53 status can determine the biological impact of vitamin D on tumor cells. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
 We thank Pubpeer for bringing this problem to our attention. We have communicated this matter to the journal and are awaiting their further instructions. Sincerely, Varda Rotter and Moshe Oren , 
null, 
 While waiting for the Biochemical Journal to decide the fate of the 3rd worst-ever paper published from the Weizmann, https: pubpeer.com publications 86E709835E96908738330ED4B849CC I couldnu2019t help but notice that a 2006 CDDif paper shares a control Weizmann ImmunoBlot (WIB) with a Cancer Cell paper published some four years later. Although the WIB is the same source image, the labelling is entirely unrelated. Will Nature Publishing Group be sending Cancer Cell a DRM takedown notice for this violation of their precious copyright? ![image] ,
Biophysical Interactions of Novel Oleic Acid Conjugate and its Anticancer Potential in HeLa Cells
Authors: Ali Saber Abdelhameed
Arun Chauhan
Rizwan Wahab
Azmat Ali Khan
Amer M Alanazi
Mumtaz Jabeen
Mohammad Khalid Parvez
Journal: Journal of fluorescence (2015)
Discipline: CHEMISTRY
Keywords: 2,6-Diisopropylphenol-Oleic acid; Anticancer activity; Protein binding; DNA binding; Toxic effect
Affiliations: Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia, .

Abstract:  Novel conjugate 2,6-Diisopropylphenol-Oleic acid (2,6P-OLA) has shown potent anticancer activity on various cancer cell lines (Khan et al. Lipids 47:973-986, 2012). In the present study, the protein-or/ and DNA-binding property of 2,6P-OLA was evaluated that could predict its potential toxic effect, in vitro. Preferential structural stability and interaction mechanism of 2,6P-OLA to human serum albumin (HSA) and calf thymus DNA (CT-DNA) was used as model molecules, employing fluorescence spectroscopy (FS) and circular dichroism (CD) methods. The binding and apoptotic activities of conjugate were determined on bacterial recombinant DNA, pBR322 and human cancer cell line, HeLa, respectively. FS studies showed a strong conjugate binding affinity to HSA with overall binding constant of K = 7.66 (±0.03) × 10(2) M(-1). Higher concentration induced detectable changes in the CD spectrum of HSA. The conjugate complexation altered HSA secondary conformation by an increase in α-helices and decrease in β-sheets. Flourescence quenching studies with CT-DNA exhibited K = 1.215 × 10(2) L mol(-1) where 2,6P-OLA efficiently displaced the ethidium bromide (EtBr) bound DNA indicating its strong competition with EtBr for intercalation. Similarly, 2,6P-OLA was able to partially bind pBR322, resulting in decrease the intensity of EtBr gradually. The conjugate significantly reduced survival of HeLa cells. Morphological studies revealed altered cell morphology, suggesting apoptotic death of HeLa cells. Overall, our data shows that 2,6P-OLA bind well with both HSA and DNA and possessed anticancer activities. 

Retracted: No

PubPeer comments:
 This article has a May 2015 correction for an incorrect author name. However, there is a potential other problem that has not yet been addressed. * Figure 2 shows the binding between 2,6P-OLA and human serum albumin (HSA). * Figure 5 shows the binding between 2,6P-OLA and EtBr-CT-DNA Both figures appear to be showing the same datapoints, albeit shown with a different X-axis and a different K value. Figure 2 has an extra datapoint not shown in the Figure 5 plot, but the distance and placement of the datapoints with respect to the line and the X Y axis values appears to be identical. Shown with red boxes. Could the authors please check? ![file] ,
PinX1 suppresses tumorigenesis by negatively regulating telomerase/telomeres in colorectal carcinoma cells and is a promising molecular marker for patient prognosis
Authors: Yihang Guo
Xi Chen
Yong Guan
Xianliang Zeng
Xiuli Chen
Minghan Qiu
Dong Qian
Huanhuan Wang
Dan Xie
Ping Wang
Qingsong Pang
Jiefu Wang
Bin Zhang
Zhiyong Yuan
Jingjing Cheng
Xiaofeng Ding
Puchun Er
Lujun Zhao
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: PinX1; apoptosis; cell proliferation; colorectal carcinoma; prognostic biomarker
Affiliations: Department of Radiotherapy., Department of Lung Cancer., Department of Colorectal Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin., State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou, People's Republic of China.

Abstract:  PinX1 plays positive and negative roles in the maintenance of telomerase and telomeres, as well as in tumorigenesis. The aim of the present study was to investigate the expression and clinical significance of PinX1 in colorectal carcinoma (CRC) and to determine the effect of PinX1 on CRC cell proliferation and apoptosis. A total of 86 CRC patients treated with radical resection and 5-fluorouracil-based adjuvant chemotherapy were enrolled in this study. The expression dynamics of PinX1 was detected by immunohistochemistry in the CRC patients and 25 normal colonic mucosa controls. PinX1 expression was significantly reduced in tumor tissues as compared to normal tissues, and the rate of PinX1 protein low/negative expression in CRC and normal tissues was 60% (52/86) and 24% (6/25), respectively (P=0.037). In addition, PinX1 downregulation was significantly associated with short overall survival (P=0.016) and disease-free survival (P=0.042) in CRC patients. Cox proportional hazards model further revealed that PinX1 expression was an independent factor in predicting overall survival and disease-free survival for CRC patients. Furthermore, we demonstrated that ectopic overexpression of PinX1 in CRC cells inhibited their proliferation, promoted apoptosis, repressed telomerase activity, and induced telomere shortening. These findings suggest that PinX1 may be a prognostic biomarker for CRC patients' survival and that it inhibits cell proliferation and promotes apoptosis by repressing telomerase activity and inducing telomere shortening. Targeting PinX1 may therefore provide a novel therapeutic strategy for CRC patients. 

Retracted: No

PubPeer comments:
 The flow cytometry plots and Figure 3 appear to have unexpected areas of similarity. One example shown. *** ![file] *** Closeup in false color ![file] ,
The effect of DASH diet on pregnancy outcomes in gestational diabetes: a randomized controlled clinical trial
Authors: Z Tabassi
Z Asemi
A Esmaillzadeh
M Samimi
Journal: European Journal of Clinical Nutrition (2014)
Discipline: CLINICAL MEDICINE
Keywords: Dietary Approaches to Stop Hypertension (DASH); pregnancy outcomes; gestational diabetes mellitus (GDM); randomized controlled clinical trial; insulin therapy
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran., Department of Gynecology and Obstetrics, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran., 1] Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran [2] Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran.

Abstract:  Background/objectives: The current study was performed to investigate the effects of the Dietary Approaches to Stop Hypertension (DASH) eating plan on pregnancy outcomes in pregnant women with gestational diabetes mellitus (GDM). Subjects/methods: This randomized controlled clinical trial was performed among 52 women diagnosed with GDM. Participants were randomly assigned to consume either the control (n=26) or the DASH diet (n=26) for 4 weeks. The control diet was designed to contain 45-55% carbohydrates, 15-20% protein and 25-30% total fat. The DASH diet was rich in fruits, vegetables, whole grains and low-fat dairy products, and contained lower amounts of saturated fats, cholesterol and refined grains with a total of 2400 mg/day sodium. The numbers of women who commenced insulin therapy after dietary intervention, the mode of delivery and prevalence of polyhydramnios were assessed. The length, weight and head circumference of infants were measured during the first 24 h after birth. Results: Whereas 46.2% of women in the DASH diet needed to have a cesarean section, this percentage for the control group was 80.8% (P=0.01). The percentage of those who needed to commence insulin therapy after intervention was also significantly different between the two groups (23% for DASH vs 73% for control group, P&lt;0.0001). Infants born to mothers on the DASH diet had significantly lower weight (3222.7 vs 3818.8 g, P&lt;0.0001), head circumference (34.2 vs 35.1 cm, P=0.01) and ponderal index (2.50 vs 2.87 kg/m(3), P&lt;0.0001) compared with those born to mothers on the control diet. Conclusions: In conclusion, consumption of DASH diet for 4 weeks among pregnant women with GDM resulted in improved pregnancy outcomes. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A16 2. Account Res 2020; 28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
<p>LINC01224 Exhibits Cancer-Promoting Activity in Epithelial Ovarian Cancer Through microRNA-485-5p-Mediated PAK4 Upregulation</p>
Authors: Shujian Xing
Jing Zhang
Yaqi Zhang
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: anticancer therapy; epithelial ovarian cancer; long intergenic non-protein coding RNA 1224; p21‑activated kinase 4.
Affiliations: Department of Gynaecology and Obstetrics, Zouping People's Hospital, Zouping, Shandong 256200, People's Republic of China., Department of Gynaecology and Obstetrics, Weifang Yidu Central Hospital, Weifang, Shandong 262500, People's Republic of China., Department of Gynaecology and Obstetrics, The No.4 Hospital of Jinan, Jinan, Shandong 250031, People's Republic of China.

Abstract:  Purpose: Long intergenic non-protein coding RNA 1224 (LINC01224) plays vital roles in the tumorigenesis and progression of hepatocellular carcinoma. Here, we determined LINC01224 expression in epithelial ovarian cancer (EOC) tissues and cells. We also assessed the effects of LINC01224 knockdown on the malignant phenotype of EOC cells both in vitro and in vivo. Furthermore, the detailed molecular mechanisms underlying the oncogenic actions of LINC01224 in EOC cells were elucidated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect LINC01224 expression in EOC tissues and cells. EOC cells were transfected with small interfering RNAs, and cell proliferation, apoptosis, migration, and invasion were assessed using Cell Counting Kit-8 assay, flow cytometry, cell migration assays, and cell invasion assays, respectively. Using tumor xenografts, the effects of LINC01224 silencing on EOC tumor growth were analyzed in vivo. The mechanism underlying LINC01224 regulation of malignant processes in EOC cells was explored using bioinformatics, RNA immunoprecipitation assay, qRT-PCR, Western blotting, and rescue experiments. Results: LINC01224 expression was upregulated in EOC tissues and cells. LINC01224 upregulation was correlated to tumor size, the International Federation of Gynecology and Obstetrics stage, and lymph node metastasis. LINC01224 depletion in EOC cells suppressed cell proliferation, migration, and invasion and facilitated cell apoptosis in vitro. LINC01224 downregulation also hindered EOC tumor growth in vivo. Mechanistically, LINC01224 served as a competing endogenous RNA for microRNA-485-5p (miR-485-5p) and consequently increased p21-activated kinase 4 (PAK4) expression in EOC cells. Furthermore, miR-485-5p inhibition or PAK4 upregulation significantly abrogated the effects of LINC01224 depletion in EOC cells. Conclusion: LINC01224/miR-485-5p/PAK4 formed a competing endogenous RNA network regulating the aggressive behavior of EOC. Therefore, targeting this pathway may be an attractive therapeutic strategy for EOC. 

Retracted: Yes

PubPeer comments:
 In Figure 6a, three tumors from two different experiments show surprisingly similarities when one of the images are rotated and flipped. ![file] , 
 Fig 5 a, c. Lots of unexpected similarities. I have marked a few. ![file] ,
Mutation and methylation analysis of the transforming growth factor beta receptor II gene in polycythaemia vera
Authors: B J Huntly
A J Bench
J Li
A R Green
Journal: British journal of haematology (2001)
Discipline: CLINICAL MEDICINE
Keywords: Polycythaemia vera; myeloproliferative disorder; TGF-beta1; TGF-beta receptor II; mutation analysis
Affiliations: Department of Haematology, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2XY, UK.

Abstract:  Polycythaemia vera (PV) is a myeloproliferative disorder (MPD) thought to result from transformation of a haemopoietic stem cell. Transforming growth factor beta1 (TGF-beta1) is a negative regulator of haemopoietic stem cells, an effect mediated by direct binding to TGF-beta receptor II (TGF-beta RII). Reduced levels of TGF-beta RII mRNA or protein have been reported in several MPDs including PV, suggesting a role for TGF-beta RII in PV. No mutational analysis of the TGF-beta RII gene has yet been performed in PV. To investigate whether genetic or epigenetic alteration of the TGF-beta RII gene contributes to the pathogenesis of PV, we performed mutation and methylation analysis in 15 PV patients. The promoter, all seven exons and all intron/exon junctions were studied using single-strand conformation polymorphism (SSCP) and heteroduplex analysis (HA). In total, three single nucleotide polymorphisms (SNPs) were identified. These were located in the promoter, intron 2 and exon 5. No acquired mutations were detected in any patient sample. We also present a novel method, termed methylation-specific strand extension (MSSE), for the detection of methylated CpG dinucleotides. The combination of bisulphite modification and MSSE permits rapid analysis of the methylation status of CpG dinucleotides in multiple samples. We analysed the methylation status of the promoter and of a CpG island within exon 1 in 15 PV patients. No aberrant methylation was detected in either of these regions. These data demonstrate that neither mutation nor abnormal methylation of the TGF-beta RII gene is associated with the pathogenesis of PV. Furthermore, MSSE is a rapid and robust approach for assessing the methylation status of a given genomic region. 

Retracted: No

PubPeer comments:
 Figure 3B. Much more similar than expected. ![file] ,
Tumor necrosis factor-related apoptosis-inducing ligand inhibits proliferation and induces apoptosis of prostate and bladder cancer cells
Authors: Cong-Hui Han
Yan Zhao
Pei-Ying Zhang
Lin Hao
Zhi-Guo Zhang
Zhi-Gang Li
Zhen-Duo Shi
Hou-Guang He
Qing Liang
Journal: Oncology Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; bladder cancer; proliferation; prostate cancer; tumor necrosis factor-related apoptosis-inducing ligand.
Affiliations: Department of Urology, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.

Abstract:  The effect of recombinant and purified tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on the proliferation and apoptosis of PC-3 prostate cancer cells and the 5637 bladder cancer cells were investigated. We used a cell proliferation assay and flow cytometry to measure the proliferation and apoptosis of cancer cells after 24-h incubation of PC-3 and 5637 cells with different concentrations of TRAIL. PC-3 cell proliferation rate significantly decreased when TRAIL was used at concentrations of 20, 40, 80 and 160 ng/ml compared with the untreated group. In the 5637 cells, the proliferation rate significantly decreased when TRAIL was used at concentrations of 5, 10, 20 and 40 ng/ml compared with the untreated group. The flow cytometry results also confirmed that the apoptosis rate of both cancer cell lines increased with TRAIL protein concentration. In conclusion, recombinant and purified TRAIL has anticancer activity by inhibiting proliferation and promoting apoptosis of prostate and bladder cancer cells. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader. * Red boxes: A panel in Figure 1 looks very similar to a panel in Figure 2. Yet, the gated percentages are different. ![file] ,
Viable offspring derived from fetal and adult mammalian cells
Authors: K H Campbell
J McWhir
A J Kind
A E Schnieke
I Wilmut
Journal: Nature (1997)
Discipline: Multidisciplinary
Keywords: Fertilization; cell divisions; differentiation; nucleus transfer; genetic modification
Affiliations: Roslin Institute (Edinburgh), Roslin, Midlothian, UK. 

Abstract:  Fertilization of mammalian eggs is followed by successive cell divisions and progressive differentiation, first into the early embryo and subsequently into all of the cell types that make up the adult animal. Transfer of a single nucleus at a specific stage of development, to an enucleated unfertilized egg, provided an opportunity to investigate whether cellular differentiation to that stage involved irreversible genetic modification. The first offspring to develop from a differentiated cell were born after nuclear transfer from an embryo-derived cell line that had been induced to become quiescent. Using the same procedure, we now report the birth of live lambs from three new cell populations established from adult mammary gland, fetus and embryo. The fact that a lamb was derived from an adult cell confirms that differentiation of that cell did not involve the irreversible modification of genetic material required for development to term. The birth of lambs from differentiated fetal and adult cells also reinforces previous speculation that by inducing donor cells to become quiescent it will be possible to obtain normal development from a wide variety of differentiated cells. 

Retracted: No

PubPeer comments:
null, 
 Yes, Nature has paid attention - they corrected this error weeks after publishing, in March 1997. Here is the link to the erratum: https: www.nature.com articles 386200a0. Here is the link to the free erratum PDF: https: www.nature.com articles 386200a0.pdf Screenshot of the erratum: ![file] ,
Rac1 activity is required for the activation of hypoxia-inducible factor 1
Authors: G L Semenza
K Hirota
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hypoxia-inducible factor 1; HIF-1; transcription factor; cellular homeostasis; erythropoiesis
Affiliations: Department of Anesthesia, Kyoto University Hospital, Kyoto University, Kyoto 606-8507, Japan.

Abstract:  Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates cellular and systemic homeostatic responses (including erythropoiesis, angiogenesis, and glycolysis) to reduced O(2) availability in mammals. Hypoxia induces both the protein expression and transcriptional activity of the HIF-1alpha subunit. However, the molecular mechanisms of sensing and signal transduction by which changes in O(2) concentration result in changes in HIF-1 activity are poorly understood. We report here that the small GTPase Rac1 is activated in response to hypoxia and is required for the induction of HIF-1alpha protein expression and transcriptional activity in hypoxic cells. 

Retracted: No

PubPeer comments:
 Figure 2A. Much more similar than expected. ![file] , 
 Figure 4A lane 3 may have an insert. https: www.jbc.org content 276 24 21166 F4.large.jpg , 
 #2 Figure 4A. Vertical changes in background in one panel, but no in the other. ![file] ,
Long non‐coding RNA UCA 1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT /β‐catenin signaling pathway
Authors: Ju-Yi Lai
Yu-Fan Wang
Jie Kong
Wei Zhang
Feng Wang
Yong-Tao Yang
Shi-Yue Shen
Hong-Yu Yang
Journal: Cancer Science (2016)
Discipline: CLINICAL MEDICINE
Keywords: Cell growth; UCA1; WNT/β-catenin pathway; cell invasion; oral squamous cell carcinoma.
Affiliations: Graduate school, Guangzhou Medical University, Guangzhou, China., Department of Oral and Maxillofacial surgery, Peking University Shenzhen Hospital, Shenzhen, China., Shenzhen TCM Hospital, Guangzhou University of Traditional Chinese Medicine, Shenzhen, China., Biomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.

Abstract:  With the development of functional genomics studies, a mass of long non-coding RNAs (LncRNA) were discovered from the human genome. Long non-coding RNAs serve as pivotal regulators of genes that are able to generate LncRNA-binding protein complexes to modulate a great number of genes. Recently, the LncRNA urothelial carcinoma-associated 1 (UCA1) has been revealed to be dysregulated, which plays a critical role in the development of a few cancers. However, the role of the biology and clinical significance of UCA1 in the tumorigenesis of oral squamous cell carcinoma (OSCC) remain unknown. We found that UCA1 expression levels were upregulated aberrantly in tongue squamous cell carcinoma tissues and associated with lymph node metastasis and TNM stage. We explored the expression, function, and molecular mechanism of LncRNA UCA1 in OSCC. In the present work, we revealed that UCA1 silencing suppressed proliferation and metastasis and induced apoptosis of OSCC cell lines in vitro and in vivo, which might be related to the activation level of the WNT/β-catenin signaling pathway. Our research results emphasize the pivotal role of UCA1 in the oncogenesis of OSCC and reveal a novel LncRNA UCA1-β-catenin-WNT signaling pathway regulatory network that could contribute to our understanding in the pathogenesis of OSCC and assist in the discovery of a viable LncRNA-directed diagnostic and therapeutic strategy for this fatal disease. 

Retracted: No

PubPeer comments:
 figure 4a and figure5b-d seems to have duplicate picturesuff0cplease check!![file] ![file] ,
MiR-1266 suppresses the growth and metastasis of prostate cancer via targeting PRMT5
Authors: G-M Zhang
S-J Cheng
M Wang
D Li
C-M Sun
M Liu
H-N Qian
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-1266; prostate cancer; PRMT5; progression; cell proliferation
Affiliations: Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. .

Abstract:  Objective: To elucidate the correlation between microRNA-1266 (miR-1266) and prostate cancer (PCa) progression, and to investigate the possible underlying mechanism. Patients and methods: The expression level of miR-1266 and protein arginine methyltransferase 5 (PRMT5) in PCa tissues and cell lines was first detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After up-regulating or down-regulating miR-1266 expression in cells, cell proliferation, migration and invasion abilities were detected. Possible target genes of miR-1266 were predicted and validated by bioinformatics analysis and dual-luciferase reporter gene assay, respectively. Finally, abnormal expression of PRMT5 was ascertained after transfection. Results: MiR-1266 was lowly expressed in PCa tissues and cell lines, whereas PRMT5 exhibited the opposite results. Up-regulated expression of miR-1266 significantly inhibited the proliferation, migration and invasion abilities of PC-3 cells. However, the growth and migration of DU145 cells with low miR-1266 expression were significantly accelerated. Meanwhile, the number of invading cells was significantly increased. PRMT5 was verified as a potential target gene of miR-1266. Furthermore, results found that miR-1266 was negatively correlated with PRMT5. In addition, the expression of PRMT5 was remarkably decreased after miR-1266 overexpression, which could be restored after knockdown of miR-1266. Conclusions: MiR-1266 inhibits the growth and metastasis of PCa by targeting PRMT5. We may provide a potential and prospective therapeutic target for PCa. 

Retracted: Yes

PubPeer comments:
 Retracted [July 2021] . --------------------------------------- The article u201cMiR-1266 suppresses the growth and metastasis of prostate cancer via targeting PRMT5, by C.-M. Sun, G.-M. Zhang, H.-N. Qian, S.-J. Cheng, M. Wang, M. Liu, D. Li, published in Eur Rev Med Pharmacol Sci 2019; 23 (15): 6436-6444u2013PMID: 31378882u201d has been withdrawn from the authors due to some inaccuracies (some data cannot be repeated by our further research). The Publisher apologizes for any inconvenience this may cause --------------------------------------------------- Table 1 shows that of the 36 cases, the number in the  low-miR-1266 expression group ranges among 17, 18, 13, 19 and 21. I would be more worried if the authors further research **had** managed to repeat this result. ![file] ,