PReD-Bench/PRed-Bench huggingface dataset:
Retracted: Oral intake of ranitidine increases urinary excretion of N-nitrosodimethylamine
Authors: William A Mitch
Teng Zeng
Journal: Carcinogenesis (2016)
Discipline: CLINICAL MEDICINE
Keywords: ranitidine; N-nitrosodimethylamine (NDMA); N-nitrosamines; stomach-relevant pH; urinary excretion
Affiliations: Department of Civil and Environmental Engineering, Syracuse University, 151 Link Hall, Syracuse, NY 13244, USA., Department of Civil and Environmental Engineering, Stanford University, 473 Via Ortega, Stanford, CA 94305, USA and., National Science Foundation Engineering Research Center for Re-Inventing the Nation's Urban Water Infrastructure (ReNUWIt), 473 Via Ortega, Stanford, CA 94305, USA.

Abstract:  The H2-receptor antagonist, ranitidine, is among the most widely used pharmaceuticals to treat gastroesophageal reflux disease and peptic ulcers. While previous studies have demonstrated that amines can form N-nitrosamines when exposed to nitrite at stomach-relevant pH, N-nitrosamine formation from ranitidine, an amine-based pharmaceutical, has not been demonstrated under these conditions. In this work, we confirmed the production of N-nitrosodimethylamine (NDMA), a potent carcinogen, by nitrosation of ranitidine under stomach-relevant pH conditions in vitro We also evaluated the urinary NDMA excretion attributable to ingestion of clinically used ranitidine doses. Urine samples collected from five female and five male, healthy adult volunteers over 24-h periods before and after consumption of 150mg ranitidine were analyzed for residual ranitidine, ranitidine metabolites, NDMA, total N-nitrosamines and dimethylamine. Following ranitidine intake, the urinary NDMA excreted over 24h increased 400-folds from 110 to 47 600ng, while total N-nitrosamines increased 5-folds. NDMA excretion rates after ranitidine intake equaled or exceeded those observed previously in patients with schistosomiasis, a disease wherein N-nitrosamines are implicated as the etiological agents for bladder cancer. Due to metabolism within the body, urinary NDMA measurements represent a lower-bound estimate of systemic NDMA exposure. Our results suggest a need to evaluate the risks attributable to NDMA associated with chronic consumption of ranitidine, and to identify alternative treatments that minimize exposure to N-nitrosamines. 

Retracted: Yes

PubPeer comments:
 https: twitter.com andrew_croxford status 1476209804666601472 ,
When Britney Spears comes to my lab
Authors: Vince LiCata
Journal: Nature (2008)
Discipline: Multidisciplinary
Keywords: pop culture; analysis; media; influence; trends

Abstract: Now that's what I call pop culture!

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2021 06 29 britney-spears-story-prompts-apology-from-nature-and-author ,
RETRACTED ARTICLE: A Complete Formula of Ocean Surface Absolute Geostrophic Current
Authors: Peter C Chu
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Absolute geostrophic current; geoid undulation; geostrophic shear; dynamic ocean topography; density
Affiliations: Naval Ocean Analysis and Prediction Laboratory, Department of Oceanography, Naval Postgraduate School, Monterey, USA. .

Abstract:  Absolute geostrophic current at the ocean surface (S) contains three components: (1) absolute geostrophic current at the geoid undulation (N), (2) geostrophic shear (between S and N) due to horizontal gradient of dynamic ocean topography, and (3) geostrophic shear (between S and N) due to horizontal gradient of density. However, only the second component is used to represent the surface absolute geostrophic current in physical oceanography and satellite geodesy. Four public datasets are used to calculate each component. Evident difference between the surface absolute geostrophic current and the second component (i.e., geostrophic shear due to horizontal gradient of dynamic ocean topography) was found by the statistical characteristics with the relative root mean square difference of 0.605. It shows that the common practice in physical oceanography and satellite geodesy is not correct. The horizontal gradient of dynamic ocean topography alone cannot be claimed as the surface absolute geostrophic current. 

Retracted: Yes

PubPeer comments:
 Copy pasted from https: www.nature.com articles s41598-021-86517-3 :  The Author has retracted this Article. In this study the Author treated the sea surface (S) and the marine geoid (N) as the two material surfaces and used the thermal wind relation between S and N to derive the formula for the ocean surface absolute geostrophic current with the intention to revise the oceanographic community s standard formula for surface geostrophic currents by allowing for nonzero flow at the level of the geoid. This approach was incorrect since the traditional formula currently used by the oceanographic community makes no such assumption, and is not derived by integrating from the geoid to the sea surface. Instead, it is derived via a direct relationship between sea surface elevation changes relative to N. The commonly-used description of the geoid as u201cthe sea surface when there is no flowu201d refers to a hypothetical situation. If the sea surface elevation (S) was governed only by geostrophy and coincided with one particular equipotential taken as the geoid, then there would be no flow on this surface. The geoid is an imaginary surface that could be either above or below the actual sea surface. An additional error was present in that the derived formula had an opposite sign in dynamic ocean topography (D) term. The Author agrees with the retraction and the wording of this retraction notice. Retraction Note. Published: 23 March 2021.  See also https: retractionwatch.com 2021 03 30 paper-about-calculating-ocean-currents-runs-aground ,
Temporal development of behavioral impairments in rats following locus coeruleus lesion induced by 6-hydroxydopamine: Involvement of β-adrenergic receptors
Authors: Reinaldo Naoto Takahashi
Katiane Roversi
Rui Daniel Prediger
Anicleto Poli
Tuane Bazanella Sampaio
Bruna Soares de Souza
Tayná Schuh
Journal: Neuropharmacology (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 6-OHDA; Apoptosis; Depression; Locus coeruleus; Memory
Affiliations: Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina (UFSC), Campus Universitário, Florianópolis, SC, Brazil., Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina (UFSC), Campus Universitário, Florianópolis, SC, Brazil. Electronic address: .

Abstract:  Noradrenergic degeneration in the locus coeruleus (LC) seems a convergent neuropathological marker of different neurodegenerative diseases. Herein, we investigated the temporal development of apoptotic signaling activation in the LC, noradrenergic dysfunction and behavioral impairments in rats following the noradrenergic lesion of the LC. For this purpose, the dopamine reuptake inhibitor nomifensine was administered 1 h before the stereotaxic bilateral injections of 6-hydroxydopamine (6-OHDA; 5, 10 or 20 μg/hem) into the LC. The behavioral and neurochemical analyses were performed at 7, 21 and 42 days after 6-OHDA injections. All doses of 6-OHDA induced neuronal death in LC, but only the highest dose (20 μg/hem) disrupted the motor function. 6-OHDA (5 μg/hem) injection induced short-term memory deficits in all periods, olfactory discrimination and long-term memory impairments at 7 days, and depressive-like behaviors at 21 and 42 days after injection. Moreover, 6-OHDA infusion increased Bax/Bcl2 ratio and caspase 3 levels, and decreased the dopamine β-hydroxylase immunocontent in the LC. Noradrenergic neurotransmission dysfunction was observed in the LC, olfactory bulb, prefrontal cortex, hippocampus and striatum. The intranasal (i.n.) noradrenaline (NA) infusion restored the impairments in the olfactory discrimination, short-term memory and depressive-like behavior of 6-OHDA-lesioned rats. In addition, these effects were blocked by the prior i.n. infusion of the β3-adrenergic receptor antagonist SR59230A. These findings indicate that the 6-OHDA injection into the LC induced the apoptosis signaling activation, noradrenergic neurotransmission dysfunction and behavioral impairments that were restored via β3-adrenergic receptors activation mediated by the i.n. NA administration. 

Retracted: No

PubPeer comments:
 ![file] ![file] ,
HPV16 oncoproteins promote cervical cancer invasiveness by upregulating specific matrix metalloproteinases
Authors: Mathurose Ponglikitmongkol
Wareerat Umnajvijit
Jarunya Ngamkham
Jittranan Kaewprag
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: matrix metalloproteinases; HPV16 oncoproteins; cervical cancer; invasion; MMP-2
Affiliations: Molecular Medicine Graduate Program, Faculty of Science, Mahidol University, Bangkok, Thailand.

Abstract:  Production of matrix metalloproteinases (MMPs) for degradation of extracellular matrix is a vital step in cancer metastasis. We investigated the effects of HPV16 oncoproteins (16E6, 16E6*I and 16E7), either individually or combined, on the transcription of 7 MMPs implicated in cervical cancer invasiveness. The levels of 7 MMPs reported to be increased in cervical cancer were determined in C33A stably expressing different HPV16 oncoproteins using quantitative RT-PCR and compared with invasion ability of cell lines using in vitro invasion and wound healing assays. Overexpression of MMP-2 and MT1-MMP was detected in HPV16E6E7 expressing cells which correlated with increased cell invasion. Combination of HPV oncoproteins always showed greater effects than its individual form. Inhibition of cell invasion using a specific MMP-2 inhibitor, OA-Hy, and anti-MT1-MMP antibody confirmed that invasion in these cells was dependent on both MMP-2 and MT1-MMP expression. Depletion of HPV16E6E7 by shRNA-mediated knock-down experiments resulted in decreased MMP-2 and MT1-MMP expression levels as well as reduced invasion ability which strongly suggested specific effects of HPV oncoproteins on both MMPs and on cell invasion. Immunohistochemistry study in invasive cervical cancers confirmed the enhanced in vivo expression of these two MMPs in HPV16-infected cells. In addition, possible sites required by HPV16E6E7 on the MMP-2 and MT1-MMP promoters were investigated and PEA3 (at -552/-540 for MMP-2, -303 for MT1-MMP) and Sp1 (at -91 for MMP-2, -102 for MT1-MMP) binding sites were shown to be essential for mediating their transactivation activity. In conclusion, our study demonstrated that HPV16E6 and E7 oncoproteins cooperate in promoting cervical cancer invasiveness by specifically upregulating MMP-2 and MT1-MMP transcription in a similar manner. 

Retracted: No

PubPeer comments:
 Concern about Figure 2B, reported to the journal in October 2015. * Green panels: Three of the 0h panels look very similar. ![file] ,
Adipocyte pseudohypoxia suppresses lipolysis and facilitates benign adipose tissue expansion
Authors: Nicholas M Morton
Christopher C West
Kenneth J Stewart
José Manuel Fernández-Real
José Maria Moreno Navarrete
Christopher J Schofield
Jonathan R Seckl
Peter J Ratcliffe
Zoi Michailidou
Journal: Diabetes (2015)
Discipline: CLINICAL MEDICINE
Keywords: Prolyl hydroxylase enzymes; PHDs; hypoxia-inducible factor; adipose; lipolysis
Affiliations: Henry Wellcome Building for Molecular Physiology, University of Oxford, Oxford, U.K. University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, U.K. ., University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, U.K., CIBERobn "Pathophysiology of Obesity and Nutrition," Biomedical Research Institute of Girona (IDIBGI), Girona, Spain., University of Edinburgh/MRC Centre for Regenerative Medicine, Edinburgh, U.K., The Department of Plastic, Reconstructive and Burns Surgery, St. Johns Hospital, Livingston, U.K., Chemistry Research Laboratory, Oxford University, Oxford, U.K., Henry Wellcome Building for Molecular Physiology, University of Oxford, Oxford, U.K.

Abstract:  Prolyl hydroxylase enzymes (PHDs) sense cellular oxygen upstream of hypoxia-inducible factor (HIF) signaling, leading to HIF degradation in normoxic conditions. In this study, we demonstrate that adipose PHD2 inhibition plays a key role in the suppression of adipocyte lipolysis. Adipose Phd2 gene ablation in mice enhanced adiposity, with a parallel increase in adipose vascularization associated with reduced circulating nonesterified fatty acid levels and normal glucose homeostasis. Phd2 gene-depleted adipocytes exhibited lower basal lipolysis in normoxia and reduced β-adrenergic-stimulated lipolysis in both normoxia and hypoxia. A selective PHD inhibitor suppressed lipolysis in murine and human adipocytes in vitro and in vivo in mice. PHD2 genetic ablation and pharmacological inhibition attenuated protein levels of the key lipolytic effectors hormone-sensitive lipase and adipose triglyceride lipase (ATGL), suggesting a link between adipocyte oxygen sensing and fatty acid release. PHD2 mRNA levels correlated positively with mRNA levels of AB-hydrolase domain containing-5, an activator of ATGL, and negatively with mRNA levels of lipid droplet proteins, perilipin, and TIP47 in human subcutaneous adipose tissue. Therapeutic pseudohypoxia caused by PHD2 inhibition in adipocytes blunts lipolysis and promotes benign adipose tissue expansion and may have therapeutic applications in obesity or lipodystrophy. 

Retracted: No

PubPeer comments:
 Figure 1. * Red arrows: Lane  C in the Acetyl-p53 looks similar to lane  BP in the b-Actin panel. ![file] ,
KIF2A silencing inhibits the proliferation and migration of breast cancer cells and correlates with unfavorable prognosis in breast cancer
Authors: Song Zhao
Jianli Wang
Wenjun Liu
Xun Qu
Siqin Ma
Rong Ma
Cuixia Lv
Yunyun Gong
Journal: BMC Cancer (2014)
Discipline: CLINICAL MEDICINE
Keywords: Kinesin family member 2a; breast cancer; tumorigenesis; progression; immunohistochemical staining
Affiliations: Department of Pathology and Pathophysiology, School of Medicine, Shandong University, 44# Wen Hua Xi Road, Jinan, Shandong, China. .

Abstract:  Background: Kinesin family member 2a (KIF2A), a type of motor protein found in eukaryotic cells, is associated with development and progression of various human cancers. The role of KIF2A during breast cancer tumorigenesis and progression was studied. Methods: Immunohistochemical staining, real time RT-PCR and western blot were used to examine the expression of KIF2A in cancer tissues and adjacent normal tissues from breast cancer patients. Patients' survival in relation to KIF2A expression was estimated using the Kaplan-Meier survival and multivariate analysis. Breast cancer cell line, MDA-MB-231 was used to study the proliferation, migration and invasion of cells following KIF2A-siRNA transfection. Results: The expression of KIF2A in cancer tissues was higher than that in normal adjacent tissues from the same patient (P &lt; 0.05). KIF2A expression in cancer tissue with lymph node metastasis and HER2 positive cancer were higher than that in cancer tissue without (P &lt; 0.05). A negative correlation was found between KIF2A expression levels in breast cancer and the survival time of breast cancer patients (P &lt; 0.05). In addition, multivariate analysis indicated that KIF2A was an independent prognostic for outcome in breast cancer (OR: 16.55, 95% CI: 2.216-123.631, P = 0.006). The proliferation, migration and invasion of cancer cells in vitro were suppressed by KIF2A gene silencing (P &lt; 0.05). Conclusions: KIF2A may play an important role in breast cancer progression and is potentially a novel predictive and prognostic marker for breast cancer. 

Retracted: No

PubPeer comments:
 image duplications between 4D and E as well as 4F and 4I ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Silencing of TCTN1 inhibits proliferation, induces cell cycle arrest and apoptosis in human thyroid cancer
Authors: Peipei Xu
Xiaotian Xia
Yuan Tian
Minggao Guo
Jianzhong Di
Zhili Yang
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: TCTN1; apoptosis; proliferation; thyroid cancer.
Affiliations: Department of Surgery, The Sixth People's Hospital of Shanghai, Shanghai Jiaotong University, Shanghai 200233, P.R. China.

Abstract:  Tectonic family member 1 (TCTN1) is one of the tectonic family members, and a regulator of the hedgehog signaling pathway, which has been studied in various cancer types, including prostate and pancreatic cancer. However, its function in thyroid cancer has not been well documented. Therefore, the present study investigated the function of TCTN1 in thyroid cancer using a loss-of-function assay. Lentivirus-mediated RNA interference was applied to downregulate TCTN1 in the thyroid cancer cell lines, CAL62 and 8305C. A series of functional properties, including cell viability, colony formation, cell cycle and apoptosis were determined using MTT, colony formation assay and flow cytometry analyses, respectively. The results demonstrated that lentivirus-medicated RNAi could specifically suppress the expression of TCTN1 at the mRNA and protein levels in CAL62, and 8305C cells. Knockdown of TCTN1 inhibited cell growth and proliferation via inducing S phase arrest, and apoptosis. Mechanistically, the S phase arrest was accompanied by the upregulation of cyclin dependent kinase 2, cyclin A2 and downregulation of cyclin B1. Knockdown of TCTN1 induced apoptosis through increasing the expression of Bcl2-associated agonist of cell death, cleaved caspase-3 and poly(ADP-ribose)polymerase, and decreasing apoptosis regulator Bcl-2 expression. The current study highlights the essential role of TCTN1 in promoting thyroid cancer cell proliferation, and its knockdown may serve as a potential therapeutic treatment for thyroid cancer. 

Retracted: No

PubPeer comments:
 Fig 2 and Fig 6 : Reuse of suspected WB experimental bands and background ![file] ![file] ,
Resveratrol downregulates interleukin-6-stimulated sonic hedgehog signaling in human acute myeloid leukemia
Authors: Li-Min Wang
Hui-Fen Liao
K S Clifford Chao
Yu-Chieh Su
Szu-Chin Li
Yin-Chi Wu
Journal: Evidence-based Complementary and Alternative Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: IL-6; sonic hedgehog; Shh signaling; cancer stem cells; CSCs
Affiliations: Department of Medicine, College of Medicine, Tzu Chi University, Hualien 97004, Taiwan ; Division of Hematology and Oncology, Department of Internal Medicine, Buddhist Dalin Tzu Chi General Hospital, Chiayi 62247, Taiwan., Division of Hematology and Oncology, Department of Internal Medicine, Buddhist Dalin Tzu Chi General Hospital, Chiayi 62247, Taiwan, Department of Biochemical Science and Technology, National Chiayi University, Chiayi 60004, Taiwan, Department of Radiation Oncology, Columbia University, New York, NY 10027, USA, Institute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan

Abstract:  IL-6 and sonic hedgehog (Shh) signaling molecules are considered to maintain the growth of cancer stem cells (CSCs). Resveratrol, an important integrant in traditional Chinese medicine, possesses certain antitumor effects. However, the mechanisms on regulating acute myeloid leukemia (AML) are unclear. This study first used human subjects to demonstrate that the plasma levels of IL-6 and IL-1 β in AML patients were higher and lower, respectively, than healthy donors. The expression of Shh preproproteins, and C- and N-terminal Shh peptides increased in bone marrow and peripheral blood mononuclear cells isolated from AML patients, and the plasma N-Shh secretion was greater. To further clarify the effect of IL-6 and resveratrol in Shh signaling, human AML HL-60 cells were tested. IL-6 upregulated Shh and Gli-1 expression and was accompanied by an increase of cell viability. Resveratrol significantly decreased CSC-related Shh expression, Gli-1 nuclear translocation, and cell viability in IL-6-treated HL-60 cells and had synergistic effect with Shh inhibitor cyclopamine on inhibiting cell growth. Conclusions. IL-6 stimulated the growth of AML cells through Shh signaling, and this effect might be blocked by resveratrol. Further investigations of Shh as a prognostic marker and resveratrol as a therapeutic drug target to CSCs in AML are surely warranted. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Morphine, but not ketamine, decreases the ratio of Th1/Th2 in CD4-positive cells through T-bet and GATA3
Authors: Wenjie Jin
Yanning Qian
Jie Sun
Mei Gao
Journal: Inflammation (2012)
Discipline: IMMUNOLOGY
Keywords: morphine; CD4-positive T cells; differentiation; transcriptional factors; PMA
Affiliations: Department of Anesthesiology, First Affiliated Hospital with Nanjing Medical University, No. 300, Guangzhou Road, Nanjing, 210029, China.

Abstract:  This study was conducted to investigate the effect of morphine on CD4-positive T cells differentiation and the transcriptional factors induced by phorbol myristate acetate (PMA) and ionomycin. CD4-positive lymphocytes separated from healthy volunteers were incubated by PMA (25 ng/ml) + ionomycin (1 μg/ml) with or without the presence of morphine, ketamine, or naloxone. Th subsets, supernatant cytokines, and transcriptional factors were detected 4 h later. Th1 and Th2 cells, levels of INF-γ, IL-2, IL-4 and the activities of T-bet and GATA3 were significantly increased after incubation with PMA and ionomycin. However, the number of Th1 cells, Th1/ Th2, the levels of INF-γ and INF-γ/IL-4, and the activities and protein levels of T-bet and GATA3 were decreased after incubation with PMA and ionomycin in the presence of morphine. Naloxone can abolish morphine's suppressive effect on Th cell differentiation. Morphine has a negative effect on Th cell balance induced by PMA and ionomycin, the mechanism is related to T-bet and GATA3. 

Retracted: No

PubPeer comments:
 Looks like more similar in figure 4A, a similar bubble in the same place after horizontal flip ![file] ,
PTENP1 acts as a ceRNA to regulate PTEN by sponging miR-19b and explores the biological role of PTENP1 in breast cancer
Authors: L-H Guo
J- Gao
W-H Luo
G-Q Huang
R-K Li
Journal: Cancer Gene Therapy (2017)
Discipline: CLINICAL MEDICINE
Keywords: long noncoding RNA; PTENP1; miR-19b; breast cancer; progression
Affiliations: Department of Clinical Laboratory, Shantou University Medical College, Shantou, Guangdong, China., Department of Clinical Laboratory, The Second People's Hospital of Baoan District of Shenzhen, Shenzhen, Guangdong, China., Department of Clinical Laboratory, People's Hospital of New District Longhua, Shenzhen, Guangdong, China.

Abstract:  This study aimed to investigate role of long noncoding RNA PTENP1 regulating PTEN expression via miR-19b to affect breast cancer (BC) progression. We measured expressions of PTENP1, miR-19b and PTEN in 65 matched BC cancerous and noncancerous tissues by quantitative real-time fluorescence PCR (qRT-PCR) and investigated the biological effects of PTENP1 in BC MDA-MB-231 cells by several in vitro experiments including CCK8, wound healing, transwell and Annexin V-FITC/PI analysis. Besides, the competing endogenous RNA (ceRNA) activity of PTENP1 on miR-19b was detected by luciferase reporter assay, and the expressions of related genes and proteins were determined by western blot assay and qRT-PCR. Increased PTENP1 and PTEN and decreased miR-19b were observed in BC tissues and cell lines. Further, PTENP1 and PTEN are direct targets of miR-19b, and overexpressed PTENP1 in MDA-MB-231 cells could supress cell proliferation, migration and invasion and promote cell apoptosis. Moreover, PTENP1 could upregulate PTEN via its ceRNA interaction on miR-19b, as well as induced the upregulation of p53 and downregulation of p-AKT. Enhanced PTENP1 could inhibit BC cell growth, metastasis and tumourigenicity by inhibiting miR-19b and facilitating PTEN in BC, thereby may represent a novel target for diagnosis and treatment of BC. 

Retracted: No

PubPeer comments:
 In Figure 4a, all the 0t micrographs are identical. The authors (and reviewers) should know that the control image is the most important. ![file] ,
Protective effect of vanillic acid in hydrogen peroxide-induced oxidative stress in D.Mel-2 cell line
Authors: Jamal S M Sabir
Suriya Rehman
Shagufta Taqvi
Nasreena Sajjad
Eijaz Ahmed Bhat
Aleem Qureshi
Irfan A Rather
Journal: Saudi Journal of Biological Sciences (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNA fragmentation; Hygrogen peroxide; Oxidative stress; Pharmaceuticals; Vanillic acid.
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, Chidambaram, Tamil Nadu, India., Life Science Institute, Zhejiang University, Hangzhou, Zhejiang 310058, PR China., Department of Biochemistry, University of Kashmir, Srinagar 190006, India., Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia., Department of Environmental Engineering, College of Engineering, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia., Department of Epidemic Disease Research, Institute for Research and Medical Consultations (IRMC), Imam Abdulrahman Bin Faisal University, 31441 Dammam, Saudi Arabia.

Abstract:  The overproduction of reactive oxygen species (ROS) causes oxidative stress, such as Hydrogen peroxide (H2O2). Acute oxidative stress is one of the main reasons for cell death. In this study, the antioxidant properties of vanillic acid- a polyphenolic compound was evaluated. Therefore, this study aims to check the effectiveness of vanillic acid in H2O2-induced oxidative stress in D. Mel-2 cell line. The efficacy was determined by biochemical tests to check the ROS production. The cytotoxicity of H2O2 and vanillic acid was checked by MTT assay. The DNA fragmentation was visualized by gel electrophoresis. Protein biomarkers of oxidative stress were analyzed by western blotting. The results depict a promising antioxidant effect of vanillic acid. The IC50 value of vanillic acid and H2O2 was found 250 μg/ml and 125 μg/ml, respectively. The catalase activity, SOF, GPx, and PC was seen less in H2O2 treated group compared with the control and vanillic acid treated group. However, the TBRAS activity was hight in H2O2 treated group. The effect of H2O2 on DNA fragmentation was high as compared with vanillic acid-treated cells. The protein expression of Hsp70, IL-6 and iNOS was seen significant in a vanillic acid-treated group as compared with H2O2 treated group. These results reinforce that at low concentration, vanillic acid could be used as an antioxidant agent in the food and pharmaceutical industries. 

Retracted: No

PubPeer comments:
 Figure 2: B and C are the same image. I ve added the red rectangles to show where I mean. Would the authors please comment? ![file] , 
 Dear Anonymous reader, I would like to thank you for pointing that out. Apologies for the silly error of having the same parts b and c. Honestly, I didn t notice it until you highlighted it. Please find attached figure 2 with correct part c. I have also notified the Journal. Nevertheless, it is not their mistake. Finally, it is the authors who approve the proof. So, for that, I again apologize for this error. Thank you once again![](http: ) ! Irfan ![](http: )![file] ,
Molecular insights of genetic variation in milk thistle (Silybum marianum [L.] Gaertn.) populations collected from southwest Iran
Authors: Karim Sorkheh
Mehrana Koohi-Dehkordi
Azam Rafizadeh
Journal: Molecular Biology Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Genetic diversity; Molecular markers; SCoT marker; Silybum marianum L..
Affiliations: Department of Agricultural Science, Payame-Noor University, P. O. Box 19395-3697, Tehran, Iran., Department of Agricultural Science, Payame-Noor University, P. O. Box 19395-3697, Tehran, Iran. ., Department of Agronomy and Plant Breeding, Faculty of Agriculture, Shahid Chamran University of Ahvaz, P. O. Box 61355/144, Ahvaz, Iran.

Abstract:  Milk thistle (Silybum marianum) is among the world's popular medicinal plants. Start Codon Targeted (SCoT) marker system was utilized to investigate the genetic variability of 80 S. marianum genotypes from eight populations in Iran. SCoT marker produced 255 amplicons and 84.03% polymorphism was generated. The SCoT marker system's polymorphism information content value was 0.43. The primers' resolving power values were between 4.18 and 7.84. The percentage of polymorphic bands was between 33.3 and 100%. The Nei's gene diversity (h) was 0.19-1.30 with an average 0.72. The Shannon's index (I) ranged from 0.29 to 1.38 with an average value of 0.83. The average gene flow (0.37) demonstrated a high genetic variation among the studied populations. The variation of 42% was displayed by the molecular variance analysis among the populations while a recorded variation of 58% was made within the populations. Current investigation suggested that SCoT marker system could effectively evaluate milk thistle genotypes genetic diversity. 

Retracted: No

PubPeer comments:
 https: imgur.com a eNKlfte ,
Downregulation of miR-3127-5p promotes epithelial-mesenchymal transition via FZD4 regulation of Wnt/β-catenin signaling in non-small-cell lung cancer
Authors: Wen Xu
Yang Yang
Bo Su
Yun Wu
Yifeng Sun
Dongfang Tang
Wen Gao
Xi Ding
Journal: Molecular Carcinogenesis (2018)
Discipline: CLINICAL MEDICINE
Keywords: EMT; NSCLC; Wnt/β-catenin; metastasis; microRNA.
Affiliations: Department of Thoracic Surgery, Huadong Hospital Affiliated to FuDan University, Shanghai, China., Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China., Central Laboratory, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.

Abstract:  MiR-3127-5p has been implicated as a tumor-suppressive microRNA (miRNA) in non-small-cell lung cancer (NSCLC) and its expression was associated with tumor recurrence and poor prognosis. The aim of this study was to determine whether miR-3127-5p regulates epithelial-mesenchymal transition (EMT) in NSCLC, and to investigate the underlying mechanisms. Using qRT-PCR, we examined the expression levels of miR-3127-5p in a cohort of primary NSCLC specimens with and without distant metastasis. We further performed a series of in vitro and in vivo experiments to investigate the effects and underlying mechanism of miR-3127-5p on EMT, cell migration, invasion, and adhesion in NSCLC. We found that metastatic NSCLC tissues showed markedly downregulated miR-3127-5p expression. Transforming growth factor-β1 (TGF-β1) treatment induced EMT in A549 and H1299 cells, and downregulation of miR-3127-5p could result in the similar effect. Mechanically, we demonstrated that frizzled-4 (FZD4) is a target gene and miR-3127-5p exerts its effects by regulating the Wnt/β-catenin signaling. In addition, the expression levels of FZD4 and miR-3127-5p were also negatively associated in both clinical and xenografted tumors. Overall, these findings suggest that downregulation of miR-3127-5p promotes EMT through activating the Wnt/FZD4/β-catenin signaling pathway and may represent a therapeutic target for NSCLC metastasis. 

Retracted: No

PubPeer comments:
 Figure 4F and 4G appear to have some image duplications for cells with different treatments. ![file] ,
LncRNA CRNDE promotes hepatocellular carcinoma cell proliferation, invasion, and migration through regulating miR-203/ BCAT1 axis
Authors: Lirong Zhang
Haiying Liang
Tiechao Jiang
Degang Ji
Chengwei Jiang
Na Liang
Bin Yang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BCAT1; CRNDE; hepatocellular carcinoma cell; miR-203; proliferation.
Affiliations: Department of Hepatopancreatobiliary Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Department of Pathology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Office of Surgical Nursing, Changchun Medical College, Changchun, Jilin, China., Department of Cardiovascular Medicine, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Department of Breast Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Department of Blood transfusion, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.

Abstract:  Objective: To investigate the impact of long noncodingRNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) on hepatocellular cancer (HCC) cell propagation, invasion, and migration by mediating miR-203/ BCAT1 axis. Methods: Microarray analysis was based on 25 pairs of HCC cancerous tissues and adjacent tissues. The expression levels of CRNDE, miR-203, and BCAT1 in HCC tissues were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The liver cell line L-02 and HCC cell lines HepG2 and Huh-7 were utilized to assess the regulatory eﬀects of CRNDE and miR-203 on HCC progression in vitro. Western blot was used to qualify BCAT1 protein expression level. Cell proliferation and apoptosis were evaluated using CCK-8 and flow cytometry analysis, whereas cell invasion and migration assay were performed by the Transwell assay. The relationship among CRNDE, miR-203, and BCAT1 was validated by dual luciferase assay. Tumor Xenograft study was established to verify the pathological effect of CRNDE on HCC development in vivo. Results: The expression levels of the CRNDE and BCAT1 were upregulated in HCC tissues and cells, whereas miR-203 was downregulated in HCC. Knockdown of CRNDE or miR-203 overexpression would inhibit HCC cell propagation and metastasis, and induced cell apoptosis. Moreover, miR-203 was negatively correlated with CRNDE, the same as miR-203 with BCAT1. Dual luciferase assay showed that miR-203 was an inhibitory target of CRNDE, and BCAT1 was directly targeted by miR-203 as well. Conclusion: LncRNA CRNDE could enhance HCC tumorgenesis by sponging miR-203 and mediating BCAT1. LncRNA CRNDE might facilitate HCC cell propagation, invasiveness, and migration through regulating miR-203/ BCAT1 axis. 

Retracted: Yes

PubPeer comments:
 ![file] , 
 How to explain the duplication in the SHIP- - IB:Akt panel? , 
 #1 Figure 7C. Much more similar than you would expect. https: imgur.com yda7lcH ,
WITHDRAWN: LncRNA TUG1 knockdown mitigates inflammatory injury induced by cigarette smoke extract in chronic obstructive pulmonary disease via miR-34c/BRD4 axis
Authors: Liyun Ye
Zeng Jing
Siyu Wu
Jing Cao
Beibei Song
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BRD4; chronic obstructive pulmonary disease; inflammatory response; lncRNA TUG1; miR-34c.
Affiliations: The Second Hospital of Hebei Medical, Shijiazhuang, China, The Fourth Hospital of Shijiazhuang Medical, Shijiazhuang, China

Abstract:  Chronic obstructive pulmonary disease (COPD) is a type of respiratory disease. The dysregulation of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) has been reported in diverse diseases. This study aimed to explore the functions and mechanism of TUG1 in COPD. The levels of TUG1 and BRD4 were significantly up-regulated, and the level of miR-34c was apparently down-regulated in COPD patients or CSE-treated BEAS-2B cells. TUG1 was verified to sponge to miR-34c, and BRD4 was validated as a target of miR-34c. TUG1 depletion or miR-34c overexpression promoted cell proliferation but restrained apoptosis, inflammatory response in CSE-treated BEAS-2B cells. MiR-34c inhibitor mitigated the inhibitory effect on cell proliferation and the promotion effects on cell apoptosis, inflammatory response in CSE-treated BEAS-2B cells induced by TUG1 silencing. Mechanistically, TUG1 modulated BRD4 expression in CSE-treated BEAS-2B cells by sponging miR-34c. TUG1 modulated BRD4 to regulate cell proliferation, cell apoptosis and inflammatory response in CSE-treated BEAS-2B cells by sponging miR-34c. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] ![file] , 
 ![](http: ) ![file] , 
 Thankyou for pointing out. Sorry for the inadvertant mistake. Could have happened during multiple revisions as both the manuscript were being communicated in the same year one after the other..will check with first author and do the needful ,
Upregulation of VEGF-A and CD24 gene expression by the tGLI1 transcription factor contributes to the aggressive behavior of breast cancer cells
Authors: X Cao
M W Dewhirst
J Geradts
H-W Lo
Journal: Oncogene (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hedgehog signaling pathway; GLI1; breast cancer; tGLI1; alternative splicing
Affiliations: Division of Surgical Sciences, Department of Surgery, Duke University School of Medicine, Durham, NC 27710, USA.

Abstract:  The Hedgehog signaling pathway is one of the most dysregulated pathways in human cancers. The glioma-associated oncogene homolog 1 (GLI1) transcription factor is the terminal effector of the Hedgehog pathway, frequently activated in human breast cancer and an emerging target of breast cancer therapy. While somatic mutations in the human GLI1 gene have never been reported in any cell or tumor type, we recently uncovered the existence of a novel alternatively spliced, truncated GLI1 (tGLI1) that has an in-frame deletion of 41 codons spanning the entire exon 3 and part of exon 4 of the GLI1 gene. Using glioblastoma models, we showed that tGLI1 has gained the ability to promote glioblastoma migration and invasion via its gain-of-function transcriptional activity. However, the pathological impact of tGLI1 on breast cancer remains undefined. Here, we report that tGLI1 is frequently expressed in human breast cancer cell lines and primary specimens we have examined to date, but is undetectable in normal breast tissues. We found for the first time that tGLI1, but not GLI1, binds to and enhances the human vascular endothelial growth factor-A (VEGF-A) gene promoter, leading to its upregulation. Consequently, tGLI1-expressing MDA-MB-231 breast cancer cells secret higher levels of VEGF-A and contain a higher propensity, than the isogenic cells with control vector and GLI1, to stimulate in vitro angiogenesis of human vascular endothelial cells. We further showed that tGLI1 has gained the ability to enhance the motility and invasiveness of breast cancer cells in a proliferation-independent manner and that this functional gain is associated with increased expression of migration/invasion-associated genes, CD24, MMP-2 and MMP-9. tGLI1 has also acquired the property to facilitate anchorage-independent growth of breast cancer cells. Collectively, our results define tGLI1 as a gain-of-function GLI1 transcription factor and a novel mediator of the behavior of clinically more aggressive breast cancer. 

Retracted: No

PubPeer comments:
 Figure 7B appears to have a repeated image. *** ![file] , 
 #1 Thank you for pointing out this oversight. We will submit an erratum request to the Journal. Hui-Wen Lo , 
 #2 Any update? , 
 #3 I submitted a correction request months ago but have never heard back from the Journal. I will send a follow-up email. Thank you for the follow-up. ,
COVID-19 Autopsies, Oklahoma, USA
Authors: Subha Ghosh
Edana Stroberg
Eric J Duval
Lisa M Barton
Sanjay Mukhopadhyay
Journal: American Journal of Clinical Pathology (2020)
Discipline: CLINICAL MEDICINE
Keywords: Acute lung injury; Autopsy; COVID-19; Coronavirus; Diffuse alveolar damage
Affiliations: Office of the Chief Medical Examiner, Oklahoma City, OK., Section of Thoracic Imaging, Imaging Institute, Cleveland Clinic, Cleveland, OH., Department of Pathology, Cleveland Clinic, Cleveland, OH.

Abstract:  Objectives: To report the methods and findings of two complete autopsies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive individuals who died in Oklahoma (United States) in March 2020. Methods: Complete postmortem examinations were performed according to standard procedures in a negative-pressure autopsy suite/isolation room using personal protective equipment, including N95 masks, eye protection, and gowns. The diagnosis of coronavirus disease 2019 (COVID-19) was confirmed by real-time reverse transcriptase polymerase chain reaction testing on postmortem swabs. Results: A 77-year-old obese man with a history of hypertension, splenectomy, and 6 days of fever and chills died while being transported for medical care. He tested positive for SARS-CoV-2 on postmortem nasopharyngeal and lung parenchymal swabs. Autopsy revealed diffuse alveolar damage and chronic inflammation and edema in the bronchial mucosa. A 42-year-old obese man with a history of myotonic dystrophy developed abdominal pain followed by fever, shortness of breath, and cough. Postmortem nasopharyngeal swab was positive for SARS-CoV-2; lung parenchymal swabs were negative. Autopsy showed acute bronchopneumonia with evidence of aspiration. Neither autopsy revealed viral inclusions, mucus plugging in airways, eosinophils, or myocarditis. Conclusions: SARS-CoV-2 testing can be performed at autopsy. Autopsy findings such as diffuse alveolar damage and airway inflammation reflect true virus-related pathology; other findings represent superimposed or unrelated processes. 

Retracted: No

PubPeer comments:
  Bacterial cultures: positive for nontoxigenic Escherichia coli, Proteus mirabilis, and Candida tropicalis  Reason of death written as 1. u201ccomplications of hepatic cirrhosisu201d with 2. renal nephrosclerosis and 3. acute bronchopneumonia - all symptoms associated [with P. mirabilis] P. mirabilis is [implicated in kidney stones] - the same fan-like crystals reported in the autopsy results. So, strange they did not make the connection to this bacterial infection - can call it  nontoxigenic ,
Distinct expression of C4.4A in colorectal cancer detected by different antibodies
Authors: Mamoru Uemura
Junichi Nishimura
Naotsugu Haraguchi
Ryota Oshiro
Masahisa Ohtsuka
Yuichiro Doki
Hirofumi Yamamoto
Masaki Mori
Tsunekazu Mizushima
Ichiro Takemasa
Journal: International journal of oncology (2013)
Discipline: CLINICAL MEDICINE
Keywords: metastasis-associated gene; C4.4A; colorectal cancer; antibodies; molecular weight

Abstract:  The metastasis-associated gene C4.4A encodes a glycolipid-anchored membrane protein expressed in several human malignancies. The present study aimed to perform a detailed assessment of C4.4A expression in colorectal cancer tissues, in terms of intra-cellular localization, intra-tumoral location and difference in molecular weight. To advance this goal, we developed three new antibodies against the C4.4A protein (two polyclonal Abs: C4.4A-119 and C4.4A-277 and one monoclonal Ab: C4.4A GPI-M) to use in addition to the two previously produced polyclonal Abs (C4.4A-81, C4.4A GPI-P). Antibody specificities were confirmed by absorption tests. Western blot analysis and immunohistochemistry showed that the C4.4A-119 and C4.4-277 Abs detected 70-kDa C4.4A, mainly in the cytoplasm, irrespective of intra-tumoral location. The C4.4A GPI-P and C4.4A GPI-M Abs reacted with the membranous ~40-kDa C4.4A, exclusively at the tumor invasive front, and each detected an identical tumor cell population. The tested antibodies showed varied C4.4A detection rates in 33 CRC tissues. The C4.4A-277 Ab yielded the highest positive rate in 29 of 33 CRC tissues (87.9%), while the C4.4A GPI-P and C4.4A GPI-M Abs each only showed 33.3% positivity. The present findings suggest that the GPI anchor signaling sequence may be essential for detecting membranous C4.4A at the invasive front of CRC tissues. 

Retracted: No

PubPeer comments:
 2016 correction which reads:  Following the publication of this article, an interested reader drew to our attention an anomaly associated with the presentation of the Fig. 2D; specifically, there appeared to have been a duplication of the same u03b2-actin control band for the G4.4A GPI-M and the Absorbed Ab (antibody) experiments. After having re-examined our original data, we realize that the same u03b2-actin control bands were inadvertently selected for the data shown in Fig. 2D, and this escaped out attention at the time. Our investigation of the data has also confirmed that the u03b2-actin bands in the lower panels were produced from simultaneously performed blots using different gels or lanes with the same HCT116 cell lysates. A corrected version of Fig. 2, containing alternative data obtained from an experiment performed in duplicate, is showin below. The error with the selection of the control data did not affect the results in this study. We sincerely apologize for this mistake, and thank the reader of our article who drew this matter to our attention. Furthermore, we regret any inconvenience this mistake has caused. Here is the original Figure 2D, with the duplication marked in red: ![file] ,
LPS Induces Hyper-Permeability of Intestinal Epithelial Cells
Authors: Michael Golosovsky
Amir Bein
Betty Schwartz
Alexander Zilbershtein
Dan Davidov
Journal: Journal of Cellular Physiology (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Necrotizing Enterocolitis; Toll like receptor 4; TLR4; Lipopolysaccharides; LPS
Affiliations: The Hebrew University of Jerusalem, School of Nutritional Sciences, Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, Rehovot, Israel., The Hebrew University of Jerusalem, The Racah Institute of Physics, Jerusalem, Israel., The Hebrew University of Jerusalem, School of Nutritional Sciences, Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, Rehovot, Israel. .

Abstract:  Necrotizing Enterocolitis (NEC) is a severe inflammatory disorder leading to high morbidity and mortality rates. A growing body of evidence demonstrate the key role of the Toll like receptor 4 (TLR4) in NEC. This membranal receptor recognizes lipopolysaccharides (LPS) from the bacterial wall and triggers an inflammatory response. The aim of the present study was to elucidate the effect of LPS on paracellular permeability known to be severely affected in NEC. IEC-18 cells were treated with LPS and the effects on morphology, paracellular permeability and their associated gene and protein expressions were measured. Our results show that LPS down regulated the expression of occludin and ZO-1 mRNAs while up regulating Cdkn1a. In addition LPS caused a significant increase in paracellular permeability and epithelial barrier damage. Finally ZO-1 protein was found to be spatially disarrayed in the intercellular junctions in response to LPS. We conclude that LPS adversely affected the functionality of the intestinal epithelial barrier suggesting a new mechanism by which bacterial infection may contribute to the development of NEC. J. Cell. Physiol. 232: 381-390, 2017. © 2016 Wiley Periodicals, Inc. 

Retracted: No

PubPeer comments:
 Figure 4. * Should plots b (Difference in SPR minima wave number) and c (Refractive index differences) look so similar? ![file] ,