PReD-Bench/PRed-Bench huggingface dataset:
The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase
Authors: Andreas W P√ºschel
Uwe Schlomann
Myriam M√ºller
Jens C Schwamborn
Reinhard F√§ssler
Journal: Journal of cell science (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: axon growth; dendrite growth; Semaphorin 3A; integrin engagement; hippocampal neurons
Affiliations: Institut f√ºr Allgemeine Zoologie und Genetik, Westfalische Wilhelms-Universit√§t M√ºnster, Schlossplatz 5, D-48149 M√ºnster, Germany.

Abstract:  The rate and direction of axon and dendrite growth depend on multiple guidance signals and growth factors. Semaphorin 3A (Sema3A) acts as a repellent for axons and attractant for dendrites. Here, we show that the requirement for integrin engagement distinguishes the response of axons and dendrites to Sema3A in hippocampal neurons. Sema3A promotes the extension of hippocampal dendrites by a pathway that requires focal adhesion kinase (FAK). The stimulation of dendrite growth and FAK phosphorylation by Sema3A depend on integrin engagement. Unlike their function as a target of Sema3A during the collapse of axonal growth cones, integrins facilitate the stimulation of dendrite extension. Conditional inactivation of the genes encoding beta1 integrin or FAK blocks the growth-promoting effect of Sema3A but not the collapse of axonal growth cones. Our results demonstrate that different pathways mediate the stimulation of dendrite growth and the collapse of axonal growth cones by Sema3A. 

Retracted: No

PubPeer comments:
 Figure 7A. * Red boxes: The left pY397 panel looks very similar to the left FAK panel.  , 
 http: retractionwatch.com 2015 07 22 there-has-been-negligence-biologist-banned-for-one-year-by-german-funding-agency , 
 #1 2020 correction. https: jcs.biologists.org content 133 2 jcs243436 There was an error in J. Cell Sci. (2009) 122, 2034-2042 (doi:10.1242 jcs.038232). A reader and the authors informed the journal that the left-hand western blots for pY397 and FAK were duplicated in Fig. 7A. The authors provided all the original data for Fig. 7 and explained that the wrong Y397 panel was used during preparation of the figure. The corrected figure is shown here. ,
Acute expression of RET/PTC induces isozyme-specific activation and subsequent downregulation of PKCepsilon in PCCL3 thyroid cells
Authors: Jeffrey A Knauf
Edna Kimura
Bin Ouyang
James A Fagin
Mickey Croyle
Journal: Oncogene (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: papillary thyroid carcinomas; protein kinase C epsilon; RET/PTC; PLCgamma; subcellular localization
Affiliations: Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Mail Location 0547, Cincinnati, OH 45267, USA. 

Abstract:  Most papillary thyroid carcinomas (PTC) have an isozyme-specific reduction of protein kinase C (PKC)epsilon, which occurs through a post-transcriptional mechanism. Here, we test whether the oncoprotein RET/PTC could be responsible for this effect, since RET/PTC rearrangements are quite prevalent in PTC and RET/PTC activates PLCgamma, an upstream modulator of PKCs. At 3 h after induction of RET/PTC1 or RET/PTC3 expression, there was evidence of PKCepsilon activation. Activation was restricted to PKCepsilon, as acute expression of RET/PTC did not change the subcellular distribution of other PKC isozymes expressed in PCCL3 cells. Prolonged RET/PTC expression (2-6 days) produced an isozyme-specific change in PKCepsilon subcellular localization and a decrease in total PKCepsilon levels. The expression of RET/PTC3(Y541F), which does not interact with PLCgamma, but signals normally through other RET effectors, had no effect on PKCepsilon distribution at any of the time points examined. However, downregulation of total PKCepsilon levels was only partially prevented by expression of RET/PTC(Y541F). Cells with decreased PKCepsilon following prolonged expression of RET/PTC were relatively resistant to doxorubicin-induced apoptosis. Based on our previous observation that PCCL3 cells expressing a dominant-negative PKCepsilon are also markedly resistant to apoptosis, we propose that selective downregulation of PKCepsilon following prolonged RET/PTC activation promotes cell survival and clonal expansion. 

Retracted: No

PubPeer comments:
  , 
 I independently came across this and have the same concern. ***  ,
Upregulation of Long Noncoding RNA (lncRNA) X-Inactive Specific Transcript (XIST) is Associated with Cisplatin Resistance in Non-Small Cell Lung Cancer (NSCLC) by Downregulating MicroRNA-144-3p
Authors: Shou-Bin Xue
Lin-Juan Tian
Wei Liu
Yong-Gang Wei
Dong-Yue Zhang
Zhi-He Zhou
Dong Wang
Yun-Ping Wu
Journal: Medical Science Monitor (2019)
Discipline: CLINICAL MEDICINE
Keywords: NSCLC; cisplatin resistance; lncRNA XIST; MDR1; chemoresistance
Affiliations: Department of Respiration, The First Peoples' Hospital of Lanzhou City, Lanzhou, Gansu, China (mainland).

Abstract:  BACKGROUND Patients with advanced non-small cell lung cancer (NSCLC) treated with cisplatin, also termed cis-diamminedichloroplatinum (CDDP) or diamminedichloroplatinum (DDP), may develop chemoresistance. This study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft. MATERIAL AND METHODS Tissue samples were from patients with NSCLC who responded cisplatin (DDP-sensitive) (n=24), patients with NSCLC unresponsive to cisplatin (DDP-resistant) (n=30), and normal lung tissue (n=25). In H460/DDP and A549/DDP cells, expression of XIST, microRNA (miR)-144-3p, MDR1, and multidrug resistance-associated protein 1 (MRP1) were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. The MTT assay measured cell survival and proliferation, a transwell assay evaluated cell migration, and flow cytometry measured apoptosis. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays examined the relationship between XIST and miR-144-3p. Tumor xenografts from A549/DDP cells were studied in BALB/c nude mice. RESULTS In tissue from patients with DDP-resistant NSCLC and the mouse A549/DDP tumor xenograft, lncRNA-XIST expression was upregulated and miR-144-3p expression was inhibited. In A549/DDP and H460/DDP cells, down-regulation of lncRNA-XIST and upregulation of miR-144-3p reduced cell survival, proliferation, migration, induced apoptosis and suppressed MDR1 and MRP1 expression. CONCLUSIONS Upregulation of lncRNA-XIST was associated with cisplatin resistance in NSCLC by downregulating miRNA-144-3p in H460/DDP and A549/DDP cells, a murine A549/DDP tumor xenograft, and human tumor tissues from patients with cisplatin-resistant NSCLC. 

Retracted: No

PubPeer comments:
 The Western blots presented in Figure 2, 4, 5 and 6 are highly questionable due to their similar blurry band appearance. Could I ask the authors to please provide the uncropped raw data with MW markers?  , 
 Fig 2F,  Cell apoptosis was examined in H460 DDP and A549 DDP cells using flow cytometry .  I am making a collection of flow-cytometry scatterplots [stylised in this particular way] . Compare, for instance, with Fig 5C of [Gong Zhu (2020)] *[retracted]*.  ,
PKA-GSK3Œ≤ and Œ≤-Catenin Signaling Play a Critical Role in Trans-Resveratrol Mediated Neuronal Differentiation in Human Cord Blood Stem Cells
Authors: A Srivastava
A R Purohit
A Pandey
D Kumar
V K Khanna
V Kumar
S Jahan
S Singh
A B Pant
C S Rajpurohit
Journal: Molecular Neurobiology (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Human umbilical cord blood stem cells; Neuronal differentiation; PKA GSK3Œ≤/Œ≤-catenin signaling; Resveratrol.
Affiliations: System Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), MG Marg, Lucknow, Uttar Pradesh, 226001, India., Academy of Scientific and Innovative Research, CSIR-IITR Campus, Lucknow, India., BBD College of Dental Sciences, BBD University, Lucknow, Uttar Pradesh, India., System Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), MG Marg, Lucknow, Uttar Pradesh, 226001, India. ., Academy of Scientific and Innovative Research, CSIR-IITR Campus, Lucknow, India. .

Abstract:  The role of resveratrol (RV), a natural polyphenol, is well documented, although its role on neurogenesis is still controversial and poorly understood. Therefore, to decipher the cellular insights of RV on neurogenesis, we investigated the potential effects of the compound on the survival, proliferation, and neuronal differentiation of human cord blood-derived mesenchymal stem cells (hCBMSCs). For neuronal differentiation, purified and characterized hCBMSCs were exposed to biological safe doses of RV (10 ŒºM) alone and in combination with nerve growth factor (NGF-50 ng). The cells exposed only to NGF (50 ng/mL) served as positive control for neuronal differentiation. The genes showing significant involvement in the process of neuronal differentiation were further funneled down at transcriptional and translational level. It was observed that RV promotes PKA-mediated neuronal differentiation in hCBMSCs by inducing canonical pathway. The studies with pharmacological inhibitors also confirmed that PKA significantly induces Œ≤-catenin expression via GSK3Œ≤ induction and stimulates CREB phosphorylation and pERK1/2 induction. Besides that, the studies also revealed that RV additionally possesses the binding sites for molecules other than PKA and GSK3Œ≤, with which it interacts. The present study therefore highlights the positive impact of RV over the survival, proliferation, and neuronal differentiation in hCBMSCs via PKA-mediated induction of GSK3Œ≤, Œ≤ catenin, CREB, and ERK1/2. 

Retracted: No

PubPeer comments:
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CADM2 inhibits human glioma proliferation, migration and invasion
Authors: Mark Johnson
Hongwei Yang
Xin Wang
Nan Liu
Pengxing Zhang
Wansheng Bai
Yingduan Cheng
Yanyang Tu
Zhen Wang
Chen Yang
Wenshi Wang
Hui Liu
Journal: Oncology Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: Malignant glioma; CADM2; cell adhesion molecules; tumor suppression; expression level
Affiliations: Department of Experimental Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China., Postdoctoral Research Station of Neurosurgery, Wuhan General Hospital of Guangzhou Command, The People's Liberation Army, Wuhan, Hubei 430064, P.R. China., Department of Neurosurgery, 323rd Hospital of The People's Liberation Army, Xi'an, Shaanxi 710054, P.R. China., Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA., Department of Neurosurgery, University of Massachusetts Medical School, Worcester, MA 01605, USA., HemaCare, Van Nuys, CA 91406, USA.

Abstract:  Malignant glioma is one of the most common malignant tumors in the brain parenchyma with a poor prognosis. Cell adhesion molecules (CADMs) immunoglobulin super family is involved in the maintenance of cell adhesion, polarity and tumor suppression. However, the role and mechanisms of CADM2 in human glioma have yet to be elucidated. Therefore, the present study evaluated the expression level of CADM2 and demonstrated that CADM2 was markedly downregulated in human glioma tissues compared with normal brain tissue and glioma cell lines, and the CADM2 expression level was significantly decreased in high‚Äëgrade glioma tissues. Overexpression of CADM2 inhibited the proliferation of glioma cell proliferation in vitro and in vivo. CADM2 also inhibited the migration and invasion of U87 and U251 cells. Furthermore, overexpression of CADM2 induced a significant decrease in the expression of G1/S transition key regulators, cyclin D1, cyclin E, cyclin‚Äëdependent kinase (CDK)2 and CDK4. Additionally, CADM2 expression was associated with alterations in epithelial‚Äëmesenchymal transition (EMT) markers, including E‚Äëcadherin and Œ≤‚Äëcatenin. Taken together, the results of the present study demonstrated that CADM2 inhibits glioma tumorigenesis by regulating the cell cycle and the EMT process, suggesting that CADM2 may be a novel potential therapeutic target in human glioma. 

Retracted: No

PubPeer comments:
 Figure 4 appears to use the same image twice for different cell lines. I have adjusted the brightness so this is more easily seen.  ,
A lysosomal switch triggers proteostasis renewal in the immortal C. elegans germ lineage
Authors: Cynthia Kenyon
K Adam Bohnert
Journal: Nature (2017)
Discipline: Multidisciplinary
Keywords: germline; proteostasis; lysosomal switch; Caenorhabditis elegans; oocytes
Affiliations: Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California 94158, USA., Calico Life Sciences, South San Francisco, California 94080, USA.

Abstract:  Although individuals age and die with time, an animal species can continue indefinitely, because of its immortal germ-cell lineage. How the germline avoids transmitting damage from one generation to the next remains a fundamental question in biology. Here we identify a lysosomal switch that enhances germline proteostasis before fertilization. We find that Caenorhabditis elegans oocytes whose maturation is arrested by the absence of sperm exhibit hallmarks of proteostasis collapse, including protein aggregation. Remarkably, sperm-secreted hormones re-establish oocyte proteostasis once fertilization becomes imminent. Key to this restoration is activation of the vacuolar H+-ATPase (V-ATPase), a proton pump that acidifies lysosomes. Sperm stimulate V-ATPase activity in oocytes by signalling the degradation of GLD-1, a translational repressor that blocks V-ATPase synthesis. Activated lysosomes, in turn, promote a metabolic shift that mobilizes protein aggregates for degradation, and reset proteostasis by enveloping and clearing the aggregates. Lysosome acidification also occurs during Xenopus oocyte maturation; thus, a lysosomal switch that enhances oocyte proteostasis in anticipation of fertilization may be conserved in other species. 

Retracted: No

PubPeer comments:
 An addendum to this article was recently published:  After our Letter was published, D. Greenstein informed us that this GLD-1 transgene probably produced a misleading GFP signal, because neither a different GLD-1::GFP transgene nor a GLD-1 antibody produced a detectable signal in the proximal oocytes of females (see ref. 2 for data and a discussion of these transgenes). His results prompted us to take an approach that was less likely to generate artefacts; namely, to tag the endogenous gld-1 gene with GFP using CRISPRu2013Cas9 technology. Using this strain, we were also unable to detect a GLD-1::GFP signal in the proximal oocytes of females (see Fig. 1, Supplementary Fig. 1 and Supplementary Methods of this Addendum). This suggests that the proteasomal activity that degrades GLD-1 in the proximal oocytes of hermaphrodites (further explored by ref. 2) may also degrade GLD-1 in the proximal oocytes of females, and something other than GLD-1 may prevent lysosomes from being acidified in the absence of sperm. This mechanism remains unresolved, and is under investigation in our laboratory.  ,
Acceptance of a COVID-19 Vaccine in Japan during the COVID-19 Pandemic
Authors: Noritoshi Fukushima
Tomoki Nakaya
Tomoya Hanibuchi
Yuko Odagiri
Takako Kojima
Hidehiro Watanabe
Shigeru Inoue
Tomoko Takamiya
Hiroyuki Kikuchi
Itaru Nakamura
Reiko Saito
Shiho Amagasa
Masaki Machida
Journal: Vaccines (2021)
Discipline: IMMUNOLOGY
Keywords: COVID-19; epidemiology; public health; vaccine; vaccine hesitancy.
Affiliations: Department of Preventive Medicine and Public Health, Tokyo Medical University, Tokyo 160-8402, Japan., Department of Infection Prevention and Control, Tokyo Medical University Hospital, Tokyo 160-0023, Japan., Department of International Medical Communications, Tokyo Medical University, Tokyo 160-0023, Japan., Division of International Health (Public Health), Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan., Graduate School of Environmental Studies, Tohoku University, Miyagi 980-0845, Japan.

Abstract:  Vaccination could be a key protective measure against coronavirus disease 2019 (COVID-19), and it is important to understand the acceptability of the COVID-19 vaccine among the general public. However, there is no study on the acceptance of a COVID-19 vaccine in Japan. Therefore, this study aimed to describe the COVID-19 vaccine acceptance and hesitancy situation in Japan and assess the factors associated with such issues. This was a cross-sectional study based on an internet survey completed by 2956 people. Participants were asked to indicate how likely they were to get vaccinated for COVID-19. In addition, the participants responded to questions regarding sociodemographic factors, attitudes, and beliefs regarding COVID-19 infection and vaccination. The proportion of participants with a high likelihood of getting a COVID-19 vaccine was 62.1%. Multiple logistic regression analysis showed that vaccine acceptance was lower among several sociodemographic groups, such as women, adults aged 20-49 years, and those with a low-income level. Several psychological factors, especially the perceived effectiveness of the COVID-19 vaccine, and willingness to protect others by getting oneself vaccinated, were associated with vaccine acceptance. Our results indicate that the perceived effectiveness of the vaccine and willingness to protect others may play an important role in the acceptance of the COVID-19 vaccine. 

Retracted: No

PubPeer comments:
 To what extent does vaccine hesitancy account for the lack of vaccinations in Japan relative to government mishandling [1]? If the authors could please offer their perspective. [1] https: www.reuters.com world asia-pacific ad-campaign-critical-japans-coronavirus-response-makes-waves-2021-05-11 , 
 Thank you for your comments. I think the major reasons for the low number of vaccinated persons in Japan as of May 2021 may be not COVID-19 vaccine hesitancy, but the low number of COVID-19 vaccines distributed in Japan. ,
Pharmacokinetics of Cyclosporine A in Chinese heart transplant recipients
Authors: Rui Jin
Hongzhang Duan
Zhen Wang
Fujun Qu
Can Zhao
Journal: Immunopharmacology and immunotoxicology (2012)
Discipline: IMMUNOLOGY
Keywords: Cyclosporine A; pharmacokinetics; heart transplant recipients; steady state concentration; plasma
Affiliations: Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.

Abstract:  Aim: To determine the steady state concentration and the pharmacokinetics of Cyclosporine A (CsA) in heart transplant recipients. Methods: A single dose of 100 mg CsA capsules twice daily was given to five heart transplant recipients of steady state. The concentrations of CsA in plasma were determined by streptavidin peroxidase fluorescent polarization immunoassay. Results: The main pharmacokinetic parameters of CsA were as follows: t(max) (1.60 ¬± 0.55) h, œÅmax(951.60 ¬± 229.20) Œºg.L-1, t1/2(6.53 ¬± 2.40) h, and AUC0 -t(5162.10 ¬± 1355.01) Œºg.h.L-1. Conclusion: The study obtained the steady state pharmacokinetic parameters of CsA in Chinese heart transplant recipients. 

Retracted: No

PubPeer comments:
 2020 expression of concern. https: www.tandfonline.com doi full 10.1080 08923973.2020.1750753 Concerns have been raised that the study described in the article did not adhere to ethical guidelines as outlined in the Declaration of Helsinki and the Declaration of Istanbul and guidance from the World Health Organization and the World Medical Association regarding the source of transplanted human organs. Specifically, the British Medical Journal Open (BMJ Open) published an article highlighting many papers in which there is concern that transplanted organs were harvested from executed prisoners in China. In response to these concerns we contacted the authors to clarify the source of the transplanted organs received by the patients described in their study. However, despite multiple attempts to contact the authors and their institutions, no response was received. The Editors of Immunopharmacology and Immunotoxicology would like to alert readers of this. We will provide an update if we receive any further information. Immunopharmacology and Immunotoxicology publishes research adhering to internationally accepted ethical standards and is committed to upholding the Declaration of Helsinki and Declaration of Istanbul. Taylor Francis endorses the ethics guidelines described by the World Health Organization (WHO) and the World Medical Association (WMA). ,
The efficacy of labetalol vs dexmedetomidine for attenuation of hemodynamic stress response to laryngoscopy and endotracheal intubation
Authors: Nagat S El-Shmaa
Ghada F El-Baradey
Journal: Journal of Clinical Anesthesia (2016)
Discipline: CLINICAL MEDICINE
Keywords: Dexmedetomidine; Hemodynamic stress response; Intubation; Labetalol; Laryngoscopy.

Abstract:  Objective: To assess the effectiveness of labetalol vs dexmedetomidine for attenuation of hemodynamic stress response to laryngoscopy and endotracheal intubation. Design: Prospective, randomized, controlled, observer-blinded study. Setting: This study was carried out in Tanta University Hospital. Patients: Ninety patients of both sexes; American Society of Anesthesiologists physical status I and II; age range from 20 to 60 years; scheduled for elective surgery under general anesthesia. Interventions: Patients were divided into 3 groups (30 each). Group A received 1 Œºg/kg of dexmedetomidine as intravenous (IV) infusion, group B received labetalol 0.25mg/kg IV, and group C received 10mL saline IV. Measurements: The groups were compared for heart rate (HR), mean arterial pressure (MAP), and rate pressure product (RPP). Hemodynamic parameters were recorded during the preinduction; after induction; at intubation; and at 1, 3, 5, 10, and 15minutes. The primary outcomes were hemodynamic changes (HR, MBP, and RPP), and the secondary outcome was propofol dose requirement for induction of general anaesthesia. Results: Significant decrease (P &lt; .05) in HR, MBP, and RPP in groups A and B in comparison with group C and in group A in comparison with group B. Just before intubation, there was a significant decrease (P &lt; .05) in HR, MBP, and RPP in groups A and B in comparison with group C. In group C, there was a significant increase in HR, MBP, and RPP at all points when compared with the baseline. In group A, the mean propofol induction dose (mg) was statistically significantly low as compared with that in groups B and C. Conclusion: Dexmedetomidine attenuates the hemodynamic stress response to laryngoscopy and intubation more effectively compared with labetalol without any deleterious effects. Furthermore, dexmedetomidine decreases dose of propofol for induction of anesthesia as guided by bispectral index. 

Retracted: No

PubPeer comments:
 Please see the following PubPeer entry for comment relating to this paper as well.... https: pubpeer.com publications C2108E85D57789CCE961E0441F653F ,
Hypothalamic POMC expression is required for peripheral insulin action on hepatic gluconeogenesis through regulating STAT3 in sepsis rats
Authors: Kaipeng Duan
Nannan Zhang
Bin Feng
Bimin Shi
Journal: Journal of Cellular and Molecular Medicine (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: POMC; hepatic gluconeogenesis; hypothalamus; peripheral insulin; sepsis.
Affiliations: Department of Endocrinology and Metabolism; The First Affiliated Hospital of Soochow University; Suzhou Jiangsu China, Department of Cardiology; The First Affiliated Hospital of Soochow University; Suzhou Jiangsu China, Department of General Surgery; The First Affiliated Hospital of Soochow University; Suzhou Jiangsu China

Abstract:  Liver injury and dysregulated glucose homoeostasis are common manifestations during sepsis. Although plenty of studies reported insulin could protect against multiple organ injuries caused by critical infections among patients, little was known about the precise mechanism. We investigated whether liver inflammatory pathway and central neuropeptides were involved in the process. In sepsis rats, hepatic IKK/NF-Œ∫B pathway and STAT3 were strongly activated, along with reduced body weight, blood glucose and suppressed hepatic gluconeogenesis (GNG). Peripheral insulin administration efficiently attenuated liver dysfunction and glucose metabolic disorders by suppressing hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC) expression, hepatic NF-Œ∫B pathway and STAT3 phosphorylation. Furthermore, knockdown of hypothalamic POMC significantly diminished protective effect of insulin on hepatic GNG and insulin-induced STAT3 inactivation, but not inflammation or IKK/NF-Œ∫B pathway. These results suggest that hepatic IKK/NF-Œ∫B pathway mediates the anti-inflammatory effect of insulin in septic rats, and peripheral insulin treatment may improve hepatic GNG by inhibiting STAT3 phosphorylation dependent on hypothalamic POMC expression. 

Retracted: No

PubPeer comments:
 It appears that a band has been used twice in Figure 8A. ***  , 
 #1 Thanks to Actinopolyspora biskrensis for his her interest and kind comments on our research. As the first author of this paper, I must admit that the two bands (STAT3 and AKT) in this figure are identical. At the same time, it is obvious that it s an unintended editing error, and neither we nor the editor were able to detect it in time during the proofing stage. We have reviewed the relevant original pictures and confirmed that this is a misuse of images, and have started to send an errata request to the editor in charge of the journal, so as not to mislead more readers. Thanks again for your concern and comments. Sincerely, Dr. Bin Feng , 
 #2 Thank you for responding. Could you please provide the uncropped scans? , 
 #3   We have re-uploaded uncropped pictures of the two bands that were misused, errata and corrections are in progress. If requested by the editor-in-chief, we will then send all original uncropped scans to the journal. Next, we will communicate more with the journal about the errata, thank you again for your concern. ,
Six2 promotes non‚Äìsmall cell lung cancer cell stemness via transcriptionally and epigenetically regulating E‚Äêcadherin
Authors: Xiaoming Yu
Yuhua Jiang
Yong Zhou
Ying Xu
Ping Cong
Huaying Hou
Journal: Cell Proliferation (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: E-cadherin; cisplatin; non-small cell lung cancer; six2; stemness.
Affiliations: Cancer Prevention Center, The Second Hospital of Shandong University, Tianqiao District, Jinan, China.

Abstract:  Objectives: The roles and related mechanisms of six2 in regulating non-small cell lung cancer (NSCLC) cells progression are unclear. This work aimed to explore the roles of six2 in NSCLC cell stemness. Materials and methods: Kaplan-Meier plotter analysis was used to examine the correlation between six2 expression and the survival of NSCLC patients. Quantitative reverse transcription PCR and Western blot were performed to detect six2 expression in clinical samples. Moreover, transwell migration, tumour spheroid formation and in vivo tumour formation assays were used to examine the effects of six2 on NSCLC cell progression. Additionally, methylation analysis was carried out to measure E-cadherin methylation level in different cells. Finally, cell viability assay was performed to explore the effects of six2 on chemotherapeutic sensitivity of NSCLC cells. Results: Lung cancer patients with a higher six2 expression level displayed a shorter overall survival. Six2 expression was higher in lung cancer tissues than in normal adjacent tissues. Additionally, six2 knockdown suppressed NSCLC cell stemness. Mechanistically, six2 overexpression inhibited epithelial marker E-cadherin expression via stimulating its promoter methylation. And E-cadherin knockdown rescued six2 knockdown-induced decrease of NSCLC cancer cell stemness. Notably, six2 knockdown enhanced cisplatin sensitivity in parental NSCLC cells and attenuated cisplatin resistance in cisplatin-resistant NSCLC cells. Conclusions: Our results suggest that six2 facilitates NSCLC cell stemness and attenuates chemotherapeutic sensitivity via suppressing E-cadherin expression. 

Retracted: No

PubPeer comments:
 Fig2E and Fig3F have duplicationuff0c  Fig6F and Fig7D have duplicationuff0c  ,
Overexpression of SNHG12 regulates the viability and invasion of renal cell carcinoma cells through modulation of HIF1Œ±
Authors: Ze-Liang Li
Wei Zhou
Zhe Zhang
Xian-Kui Liu
Da-Xin Gong
Jun Li
Shu-Qi Du
Qiguang Chen
Jian-Bin Bi
Chui-Ze Kong
Zhen-Hua Li
Journal: Cancer Cell International (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HIF1Œ±; Long non-coding RNA; MiR-199a-5p; Renal cancer; SNHG12.
Affiliations: 1Department of Urology, The First Affiliated Hospital of China Medical University, No.155 Nanjing Street, Shenyang, 110001 Liaoning People's Republic of China., 2Department of Diagnostic Radiology, General Hospital of Shenyang Military Region, No.83, Wenhua Road, Shenyang, 110016 Liaoning People's Republic of China.

Abstract:  Background: Cumulative evidences demonstrated the aberrant overexpression of Small Nucleolar RNA Host Gene 12 (SNHG12) in diverse human cancer. However, the expression status and involvement of SNHG12 in renal cell carcinoma is still elusive. Methods: The expression of SNHG12 was determined by q-PCR. The transcriptional regulation was interrogated by luciferase reporter assay. Cell viability was measured with CCK-8 kit. The anchorage-independent was evaluated by soft agar assay. Cell apoptosis was analyzed by Annexin V/7-AAD double staining. The migration and invasion were determined by trans-well assay and wound scratch closure. The in vivo tumor growth was monitored in xenograft mice model. Protein expression was quantified by immunoblotting. Results: SNHG12 was aberrantly up-regulated in renal carcinoma both in vivo and in vitro. High expression of SNHG12 associated with poor prognosis. Deficiency of SNHG12 significantly suppressed cell viability, anchorage-independent growth and induced apoptosis. In addition, SNHG12 silencing inhibited migrative and invasive in vitro and xenograft tumor growth in vivo. Mechanistically, SNHG12 modulated HIF1Œ± expression via competing with miR-199a-5p, which consequently contributed to its oncogenic potential. MiR-199a-5p inhibition severely compromised SNHG12 silencing-elicited tumor repressive effects. Conclusion: Our data uncovered a crucial role of SNHG12-miR-199a-5p-HIF1Œ± axis in human renal cancer. 

Retracted: No

PubPeer comments:
 In Figure 3a and c, a transwell chamber image has been duplicated and presented as something else.  ,
Brain Injury and Impact Characteristics
Authors: Graham Walker
Parisa Saboori
Journal: Annals of Biomedical Engineering (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Impact energy; Jerk; TBI; Trapezoidal profile.
Affiliations: Department of Mechanical Engineering, Manhattan College, Bronx, NY, USA. ., Department of Mechanical Engineering, Manhattan College, Bronx, NY, USA.

Abstract:  Almost all studies of traumatic brain injuries have only focused on the maximum acceleration associated with the impact. However, it has been noted that other impact characteristics should also be considered. This study has examined the effect on brain deformation [maximum principal strain (MPS)] associated with changing three characteristics of an isosceles trapezoid acceleration profile: initial slope (jerk), maximum acceleration, and impact energy (maximum velocity squared). This involved using a preexisting finite element model of the brain and applying the trapezoidal acceleration impact to the center of the forehead. The results showed the largest values of MPS were found along a line between the coup and contrecoup positions, and that a strong direct relationship existed between maximum acceleration and brain deformation as measured using MPS. In addition, a strong direct relationship was found to exist between impact energy and brain deformation as measured using MPS. However, it was found that there was almost no observable change in MPS with respect to different jerk values, and in fact there was a slight decrease in MPS as jerk values increased. This comported with a shock spectrum analysis of a simple one dimensional multiple degree of freedom system exposed to similar trapezoidal impulses. 

Retracted: No

PubPeer comments:
 Duplications without proper citations! 2019)  2013)  2011)  , 
 **Duplication and Materials Recycling!**   , 
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Increased Gut Redox and Depletion of Anaerobic and Methanogenic Prokaryotes in Severe Acute Malnutrition
Authors: R√©gis Guieu
Niokhor Dione
Matthieu Million
Aldiouma Diallo
Vincent Lombard
Philippe Parola
Catherine Robert
Jean-Christophe Lagier
Souleymane Brah
Fabrice Armougom
Alexandre Fabre
Cheikh Sokhna
Julien Fromonot
Bernard Henrissat
Maryam Tidjani Alou
Caroline Michelle
Perrine Hugon
Didier Raoult
Dipankar Bachar
Saber Khelaifia
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Severe acute malnutrition; gut microbiota; redox potential; anaerobes; antioxidants
Affiliations: Aix-Marseille Universit√©, Unit√© de Recherche sur les Maladies Infectieuses et Tropicales Emergentes, UM63, CNRS 7278, IRD 198, INSERM 1095, Marseille, France., H√¥pital National de Niamey, Niamey, Niger., Centre National de la Recherche Scientifique, UMR 7257, 13288 Marseille, France., Aix-Marseille Universit√©, Architecture et Fonctions des Macromol√©cules Biologiques, 163, avenue de Luminy, 13288 Marseille cedex 9, France., Laboratoire de Biochimie, h√¥pital de la Timone, UMR MD2, IRBA, Marseille, France., Institut de Recherche pour le D√©veloppement (IRD), URMITE, Dakar, S√©n√©gal., Service de p√©diatrie multidisciplinaire, h√¥pital de la Timone Enfant, APHM, Marseille France., UMR_S 910, Aix-Marseille Universit√©, Marseille, France., Department of Biological Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.

Abstract:  Severe acute malnutrition (SAM) is associated with inadequate diet, low levels of plasma antioxidants and gut microbiota alterations. The link between gut redox and microbial alterations, however, remains unexplored. By sequencing the gut microbiomes of 79 children of varying nutritional status from three centers in Senegal and Niger, we found a dramatic depletion of obligate anaerobes in malnutrition. This was confirmed in an individual patient data meta-analysis including 107 cases and 77 controls from 5 different African and Asian countries. Specifically, several species of the Bacteroidaceae, Eubacteriaceae, Lachnospiraceae and Ruminococceae families were consistently depleted while Enterococcus faecalis, Escherichia coli and Staphylococcus aureus were consistently enriched. Further analyses on our samples revealed increased fecal redox potential, decreased total bacterial number and dramatic Methanobrevibacter smithii depletion. Indeed, M. smithii was detected in more than half of the controls but in none of the cases. No causality was demonstrated but, based on our results, we propose a unifying theory linking microbiota specificity, lacking anaerobes and archaea, to low antioxidant nutrients, and lower food conversion. 

Retracted: No

PubPeer comments:
 Something is terrible wrong with the data presented in Figure 5. The tumor sizes showed in Figure 5A are wrong and do not correspond to the acutal tumor size shown in Figure 5B. The tomor sizes in Figure 5B are extreme and are far above the maximum size limit in ethical guidelines. In addition two micrographs have been duplicated and presented as something else in Figure 8.  ,
Antitumor activity of monomethoxy poly(ethylene glycol)-poly (Œµ-caprolactone) micelle-encapsulated doxorubicin against mouse melanoma
Authors: Zhengyu Li
Qian Zhong
Shengtao Zhou
Zhiyong Qian
Xiang He
Xia Zhao
Xiancheng Chen
Lan Zheng
Tao Yi
Lina Zhou
Yuquan Wei
Maling Gou
Journal: Oncology Reports (2011)
Discipline: CLINICAL MEDICINE
Keywords: Doxorubicin; MPEG-PCL micelle; cytotoxicity; cellular uptake; antitumor activity
Affiliations: Department of Gynecology and Obstetrics, West China Second Hospital, Sichuan University, No 20, Section 3, South People's Road, Chengdu, Sichuan, PR China.

Abstract:  Doxorubicin (Dox) is one of the most commonly used and highly effective antineoplastic agents, but the clinical application of this broad spectrum drug is largely hampered by its poor stability and serious toxicity to normal tissues. Hence, it is essential to improve the therapeutic effect and decrease the systematic toxicity for the administration of doxorubicin. In our study, doxorubicin was incorporated into monomethoxy poly(ethylene glycol)-poly(Œµ-caprolactone) (MPEG-PCL) micelle by a self-assembly method. The cytotoxicity and cellular uptake efficiency of Dox-loaded MPEG-PCL (Dox/MPEG-PCL) micelle against B16-F10 murine melanoma cells was examined by the methylthiazoltetrazolium (MTT) test and flow cytometry. The antitumor activity of Dox/MPEG-PCL was evaluated in C57BL/6 mice injected subcutaneously with B16-F10 cells. Toxicity was evaluated in tumor-free mice. Meanwhile, tumor proliferation, intratumoal angiogenesis and apoptotic cells were evaluated by PCNA, CD31 staining and TUNEL assay, respectively. Encapsulation of doxorubicin in MPEG-PCL micelle improved the cytotoxicity of doxorubicin and enhanced its cellular uptake on B16-F10 cell in vitro. Administration of Dox/MPEG-PCL micelle resulted in significant inhibition (75% maximum inhibition relative to controls) in the growth of B16-F10 tumor xenografts and prolonged the survival of the treated mice (P&lt;0.05). These anti-tumor responses were associated with marked increase of tumor apoptosis and notable reduction of cell proliferation and intratumoral microvessel density (P&lt;0.05). The system toxicity also decreased in the Dox/MPEG-PCL group compared with free doxorubicin group. Our data indicate that the encapsulation of doxorubicin in MPEG-PCL micelle improved the anti-tumor activity in vivo without conspicuous systemic toxic effects. 

Retracted: No

PubPeer comments:
 Figure 6A and Figure 6B appear to have two images which overlap.  ,
Cytokine-induced killer cell delivery enhances the antitumor activity of oncolytic reovirus
Authors: Cariad Chester
Weiwei Ouyang
Shiqi Long
Nianxue Wang
Xing Zhao
Zhixu He
Journal: PLoS ONE (2017)
Discipline: Multidisciplinary
Keywords: Oncolytic viruses; cancer treatment; immune response; reovirus; cytokine-induced killer cells
Affiliations: Stem Cell and Tissue Engineering Research Center, Guizhou Medical University, Guiyang, Guizhou, China., Department of Immunology, Guizhou Medical University, Guiyang, Guizhou, China., Department of Thoracic Oncology, Affiliated Hospital of Guizhou Medical University, and Guizhou Cancer Hospital, Guiyang, Guizhou, China., Department of Medicine, Division of Oncology, Stanford University, Stanford, California, United States of America.

Abstract:  Oncolytic viruses (OV) have recently emerged as a promising therapeutic modality in cancer treatment. OV selectively infect and kill tumor cells, while sparing untransformed cells. The direct cytotoxic effects combined with the capacity to trigger an immune response make OV an appealing combination partner in the burgeoning field of cancer immunotherapy. One of the leading OV therapeutic candidates is the double-stranded RNA virus reovirus. In order to improve the oncolytic activity of reovirus and allow for systemic administration despite the prevalence of neutralizing antibodies, cytokine-induced killer (CIK) cells were explored as cell carriers for reovirus delivery. In this study, CIK cells were successfully loaded with reovirus ex vivo, and viral replication was limited in CIK cells. Confocal microscopy and flow cytometry demonstrated that CIK cells retained reovirus on the surface. Moreover, CIK cells could promote reovirus infection of tumor cells in the presence of neutralizing antibodies; meanwhile, cytotoxicity of CIK cells was increased after loading with reovirus. These findings support further investigation of reovirus and CIK combination for antitumor therapy. 

Retracted: No

PubPeer comments:
 Figure 2A appears to have images which overlap (magenta boxes), although the reovirus staining appears different in the merged images (yellow boxes). Note: the previous correction was to add missing funding information. ***  ,
DecOT: Bulk Deconvolution With Optimal Transport Loss Using a Single-Cell Reference
Authors: Xiuqin Liu
Liang Ma
Gan Liu
Journal: Frontiers in Genetics (2022)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: bulk RNA sequencing; cell-type deconvolution; optimal transport; single-cell RNA sequencing; wasserstein distance.
Affiliations: Department of Information and Computing Science, University of Science and Technology Beijing, Beijing, China., Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

Abstract:  Tissues are constituted of heterogeneous cell types. Although single-cell RNA sequencing has paved the way to a deeper understanding of organismal cellular composition, the high cost and technical noise have prevented its wide application. As an alternative, computational deconvolution of bulk tissues can be a cost-effective solution. In this study, we propose DecOT, a deconvolution method that uses the Wasserstein distance as a loss and applies scRNA-seq data as references to characterize the cell type composition from bulk tissue RNA-seq data. The Wasserstein loss in DecOT is able to utilize additional information from gene space. DecOT also applies an ensemble framework to integrate deconvolution results from multiple individuals' references to mitigate the individual/batch effect. By benchmarking DecOT with four recently proposed square loss-based methods on pseudo-bulk data from four different single-cell data sets and real pancreatic islet bulk samples, we show that DecOT outperforms other methods and the ensemble framework is robust to the choice of references. 

Retracted: No

PubPeer comments:
 Fails to cite relevant literature regarding optimal transport for transcriptomic data. https: www.cell.com cell pdf S0092-8674(19)30039-X.pdf https: www.biorxiv.org content 10.1101 2020.04.28.066787v2.full https: academic.oup.com bioinformatics advance-article doi 10.1093 bioinformatics btac084 6528312 https: arxiv.org abs 2102.01218 ,
EBV encoded miRNA BART8-3p promotes radioresistance in nasopharyngeal carcinoma by regulating ATM/ATR signaling pathway
Authors: Lingzhi Wang
Dehua Wu
Yanling Lin
Ying Tang
Ye Li
Jialing Zheng
Longmei Cai
Chengdong Liu
Xiaohan Zhou
Journal: Bioscience reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATM/ATR; DSBs; EBV-miR-BART8-3p; NPC; radioresistance.
Affiliations: Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China., Second Clinical Medical College, Zhujiang Hospital, Southern Medical University, Guangzhou, China., Department of Obstetrics and Gynaecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China., Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China, Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China  .

Abstract:  Resistance to radiotherapy is one of the main causes of treatment failure in patients with nasopharyngeal carcinoma (NPC). Epstein-Barr virus (EBV) infection is an important factor in the pathogenesis of NPC, and EBV-encoded microRNAs (miRNAs) promote NPC progression. However, the role of EBV-encoded miRNAs in the radiosensitivity of NPC remains unclear. Here, we investigated the effects of EBV-miR-BART8-3p on radiotherapy resistance in NPC cells in vitro and in vivo, and explored the underlying molecular mechanisms. Inhibitors of ataxia telangiectasia mutated (ATM)/ataxia telangiectasia mutated and Rad3-related (ATR) (KU60019 and AZD6738, respectively) were used to examine radiotherapy resistance. We proved that EBV-miR-BART8-3p promoted NPC cell proliferation in response to irradiation in vitro and associated with the induction of cell cycle arrest at the G2/M phase, which was a positive factor for the DNA repair after radiation treatment. Besides, EBV-miR-BART8-3p could increase the size of xenograft tumors significantly in nude mice. Treatment with KU60019 or AZD6738 increased the radiosensitivity of NPC by suppressing the expression of p-ATM and p-ATR. The present results indicate that EBV-miR-BART8-3p promotes radioresistance in NPC by modulating the activity of ATM/ATR signaling pathway. 

Retracted: No

PubPeer comments:
 There appears to be a repeated band in figure 5A. *** Closeup: HONE1 (top) 5-8F (bottom)  *** Full figure  ,
Prevalence of SARS-CoV-2 Infection in Children Without Symptoms of Coronavirus Disease 2019
Authors: Ana Marija Sola
Kristina W Rosbe
Atsuko Baba
Abel P David
Lynn Ramirez-Avila
Dylan K Chan
Journal: JAMA Pediatrics (2020)
Discipline: CLINICAL MEDICINE
Keywords: cohort study; positive test results; severe acute respiratory syndrome coronavirus 2; children; symptoms
Affiliations: University of California, San Francisco School of Medicine, San Francisco, San Francisco, Department of Otolaryngology‚ÄìHead and Neck Surgery, University of California, San Francisco, San Francisco, Division of Pediatric Otolaryngology, Department of Otolaryngology‚ÄìHead and Neck Surgery, University of California, San Francisco, San Francisco, Division of Pediatric Anesthesiology, Department of Anesthesiology, University of California, San Francisco, San Francisco, Division of Pediatric Infectious Diseases and Global Health, Department of Pediatrics, University of California, San Francisco, San Francisco

Abstract:  This cohort study examines the rate of positive test results for severe acute respiratory syndrome coronavirus 2 in children without symptoms who were treated in US hospitals for other conditions. 

Retracted: No

PubPeer comments:
 Link to full text: https: iopscience.iop.org article 10.1088 1755-1315 877 1 012045 pdf Dear Raid Hussian, **Any particular reason as to why 40 out of the 66 papers (i.e. 60%) that you cite in your work are papers co-authored by Dr Khalid Hashim, who** as per the Conference s Peer review declaration (see https: iopscience.iop.org article 10.1088 1755-1315 877 1 011002 ) **happens to be responsible for the conference s peer review process ? ** **In fact most references are to works by authors from Liverpool John Moores University (e.g Dr. Kot, Dr. Muradov etc) - same affiliation as Dr. Hashim. Would you please explain this?** Thank you.   , 
 This volume now has an Expression of Concern:  This volume and all papers within it are currently under investigation following allegations of excessive self-citation. IOP Publishing are investigating in line with the COPE guidelines and will remove or update this notice upon completion of the investigation. ,