PReD-Bench/PRed-Bench huggingface dataset:
MiR-181b-5p downregulates NOVA1 to suppress proliferation, migration and invasion and promote apoptosis in astrocytoma
Authors: Rong Wang
Feng Zhi
Naiyuan Shao
Yilin Yang
Xiwei Xia
Qiang Wang
Danni Deng
Suinuan Wang
Lian Xue
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: MicroRNAs; miR-181b-5p; Astrocytoma; Oncogenes; Tumor suppressors
Affiliations: Modern Medical Research Center, Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China., Department of Neurosurgery, Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.

Abstract:  MicroRNAs (miRNAs) are small, short noncoding RNAs that modulate the expression of numerous genes by targeting their mRNA. Numerous abnormal miRNA expression patterns are observed in various human malignancies, and certain miRNAs can act as oncogenes or tumor suppressors. Astrocytoma, the most common neuroepithelial cancer, represents the majority of malignant brain tumors in humans. In our previous studies, we found that the downregulation of miR-181b-5p in astrocytomas is associated with a poor prognosis. The aim of the present study was to investigate the functional role of miR-181b-5p and its possible target genes. miR-181b-5p was significantly downregulated in astrocytoma specimens, and the reduced expression of miR-181b-5p was inversely correlated with the clinical stage. The ectopic expression of miR-181b-5p inhibited proliferation, migration and invasion and induced apoptosis in astrocytoma cancer cells in vitro. The NOVA1 (neuro-oncological ventral antigen 1) gene was further identified as a novel direct target of miR-181b-5p. Specifically, miR-181b-5p bound directly to the 3'-untranslated region (UTR) of NOVA1 and suppressed its expression. In clinical specimens, NOVA1 was overexpressed, and its protein levels were inversely correlated with miR-181b-5p expression. Furthermore, the changing level of NOVA1 was significantly associated with a poor survival outcome. Similar to restoring miR-181b-5p expression, downregulating NOVA1 inhibited cell growth, migration and invasion. Overexpression of NOVA1 reversed the inhibitory effects of miR-181b-5p. Our results indicate that miR-181b-5p is a tumor suppressor in astrocytoma that inhibits tumor progression by targeting NOVA1. These findings suggest that miR-181b-5p may serve as a novel therapeutic target for astrocytoma. 

Retracted: No

PubPeer comments:
 The references cited are irrelevant from the beginning of this paper, e.g, ref[1] is about ecological planning but not innovation.    ,
Management and Treatment of Human Lice
Authors: Abdoul Karim Sangar√©
Ogobara K Doumbo
Didier Raoult
Journal: BioMed Research International (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: body louse; pediculosis; treatment; epidemics; lice infestation
Affiliations: Research Unit on Emerging Infectious and Tropical Diseases (URMITE), UMR CNRS 7278, IRD 198, INSERM 1095, Faculty of Medicine, Aix-Marseille University, 27 boulevard Jean Moulin, 13005 Marseille, France; Epidemiology Department of Parasitic Diseases, Faculty of Medicine and Odonto-Stomatology, Faculty of Pharmacy (MRTC/DEAP/FMOS-FAPH) UMI3189, University of Sciences, Techniques and Technologies of Bamako (USTTB), Bamako, Mali., Epidemiology Department of Parasitic Diseases, Faculty of Medicine and Odonto-Stomatology, Faculty of Pharmacy (MRTC/DEAP/FMOS-FAPH) UMI3189, University of Sciences, Techniques and Technologies of Bamako (USTTB), Bamako, Mali., Research Unit on Emerging Infectious and Tropical Diseases (URMITE), UMR CNRS 7278, IRD 198, INSERM 1095, Faculty of Medicine, Aix-Marseille University, 27 boulevard Jean Moulin, 13005 Marseille, France.

Abstract:  Of the three lice (head, body, and pubic louse) that infest humans, the body louse is the species involved in epidemics of louse-borne typhus, trench fever, and relapsing fever, but all the three cause pediculosis. Their infestations occur today in many countries despite great efforts to maintain high standards of public health. In this review, literature searches were performed through PubMed, Medline, Google Scholar, and EBSCOhost, with key search words of "Pediculus humanus", "lice infestation", "pediculosis", and "treatment"; and controlled clinical trials were viewed with great interest. Removing lice by hand or with a lice comb, heating infested clothing, and shaving the scalp were some of the oldest methods of controlling human lice. Despite the introduction of other resources including cresol, naphthalene, sulfur, mercury, vinegar, petroleum, and insecticides, the numbers of lice infestation cases and resistance have increased. To date, viable alternative treatments to replace insecticides have been developed experimentally in vitro. Today, the development of new treatment strategies such as symbiotic treatment and synergistic treatment (antibiotics + ivermectin) in vitro has proved effective and is promising. Here, we present an overview on managing and treating human lice and highlight new strategies to more effectively fight pediculosis and prevent resistance. 

Retracted: No

PubPeer comments:
 The authors declare no conflict of interest in the paper. This paper elaborates on the treatment of lice with ivermectin. However, we can note that one of author is the funder of a pharmaceutical company called Arthrobac Pharma. The scope of this pharmaceutical company is to treat lices with ivermectin as shown in this poster. Can the author explain if he still had any interest in this pharmaceutical company when the manuscript was submitted? (HTTPS: pubpeer.com storage image-1617569003770.png) ,
Activation of GPR40 induces hypothalamic neurogenesis through p38- and BDNF-dependent mechanisms
Authors: Natalia F Mendes
Guilherme A Nogueira
Carina S Solon
Alexandre Moura-Assis
Ariane M Zanesco
Vanessa C D Bobbo
Licio A Velloso
Daiane F Engel
Trond Ulven
Athanasios Papangelis
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Hypothalamic adult neurogenesis; fatty acids; GPR40; neurogenic activity; cell proliferation
Affiliations: Laboratory of Cell Signaling and Obesity and Comorbidities Research Center, University of Campinas, Campinas, SP, 13084-970, Brazil. ., Laboratory of Cell Signaling and Obesity and Comorbidities Research Center, University of Campinas, Campinas, SP, 13084-970, Brazil., Department of Drug Design and Pharmacology, University of Copenhagen, 2100, Copenhagen, Denmark.

Abstract:  Hypothalamic adult neurogenesis provides the basis for renewal of neurons involved in the regulation of whole-body energy status. In addition to hormones, cytokines and growth factors, components of the diet, particularly fatty acids, have been shown to stimulate hypothalamic neurogenesis; however, the mechanisms behind this action are unknown. Here, we hypothesized that GPR40 (FFAR1), the receptor for medium and long chain unsaturated fatty acids, could mediate at least part of the neurogenic activity in the hypothalamus. We show that a GPR40 ligand increased hypothalamic cell proliferation and survival in adult mice. In postnatal generated neurospheres, acting in synergy with brain-derived neurotrophic factor (BDNF) and interleukin 6, GPR40 activation increased the expression of doublecortin during the early differentiation phase and of the mature neuronal marker, microtubule-associated protein 2 (MAP2), during the late differentiation phase. In Neuro-2a proliferative cell-line GPR40 activation increased BDNF expression and p38 activation. The chemical inhibition of p38 abolished GPR40 effect in inducing neurogenesis markers in neurospheres, whereas BDNF immunoneutralization inhibited GPR40-induced cell proliferation in the hypothalamus of adult mice. Thus, GPR40 acts through p38 and BDNF to induce hypothalamic neurogenesis. This study provides mechanistic advance in the understating of how a fatty acid receptor regulates adult hypothalamic neurogenesis. 

Retracted: No

PubPeer comments:
 **Figure 1.** In the center of panel B most Sox2+ BrdU+ cells are inside the third ventricle (it is shown delimitated by a layer of ependymal cells (Sox2+ DAPI). Maybe this is an artifact, as ventricles are characterized of being completely devoid of cells (except for cells of choroid plexus, but they are not located in the studied region).  , 
 Indeed, there should not be cells in the ventricle itself. It is hard to say, but perhaps these are ependymal cells that detached from the lining of the ventricle? ,
Parkinson-related parkin reduces Œ±-Synuclein phosphorylation in a gene transfer model
Authors: Charbel Eh Moussa
Gw Rebeck
Sonya B Dumanis
Preeti J Khandelwal
Hilal A Lashuel
Li Rebekah Feng
Kathleen Maguire-Zeiss
Journal: Molecular neurodegeneration (2010)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Œ±-Synuclein; Parkin; Parkinson's disease; Lewy bodies; Synucleinopathies
Affiliations: Department of Neuroscience, Georgetown University Medical Center, Washington D,C, U,S,A, 20007. .

Abstract:  Background: Œ±-Synuclein aggregates in Lewy bodies and plays a central role in the pathogenesis of a group of neurodegenerative disorders, known as "Synucleinopathies", including Parkinson's disease. Parkin mutations result in loss of parkin E3-ubiquitin ligase activity and cause autosomal recessive early onset parkinsonism. Results: We tested how these two genes interact by examining the effects of parkin on post-translational modification of Œ±-Synuclein in gene transfer animal models, using a lentiviral gene delivery system into the striatum of 2-month old male Sprague Dawley rats.Viral expression of wild type Œ±-Synuclein caused accumulation of Œ±-Synuclein and was associated with increased cell death and inflammation. Œ±-Synuclein increased PLK2 levels and GSK-3Œ≤ activity and increased the levels of phosphorylated Œ±-Synuclein and Tau. Parkin co-expression reduced the levels of phosphorylated Œ±-Synuclein and attenuated cell death and inflammation. Parkin reduced PLK2 levels and increased PP2A activation. Conclusions: These data suggest that parkin reduces Œ±-Synuclein levels and alters the balance between phosphatase and kinase activities that affect the levels of phosphorylated Œ±-Synuclein. These results indicate novel mechanisms for parkin protection against Œ±-Synuclein-induced toxicity in PD. 

Retracted: No

PubPeer comments:
 unexpected image duplication  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. ,
The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation
Authors: Ya Wang
Hongyan Wang
Xiang Wang
Piyan Zhang
Journal: DNA repair (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ionizing radiation; DNA double strand breaks; non-homologous end-joining; homologous recombination repair; Ku-dependent pathway
Affiliations: Department of Radiation Oncology and Kimmel Cancer Center of Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Abstract:  Ionizing radiation (IR) induced DNA double strand breaks (DSBs) are repaired by both non-homologous end-joining (NHEJ) and homologous recombination repair (HRR) in mammalian cells. The NHEJ repair includes a Ku-dependent main pathway and a PARP-1-dependent complementary pathway. Compared with low linear energy transfer (LET) IR (X or gamma ray) at the same doses, high LET IR (high-charge particles) induces more cell death because of ineffective DNA repair. However, it remains unclear whether high LET IR inhibits all repair or specifically one repair pathway. By combining the assays of clonogenic survival, G2M checkpoint and gammaH2AX in the cell lines with deficiencies in different repair genes, we show here that high LET IR inhibits only the Ku-dependent main NHEJ pathway and does not inhibit either the HRR pathway or the PARP-1-dependent complementary NHEJ pathway. In addition, by developing an assay to detect small fragments of DSB (&lt;400 bp) and by detecting the binding abilities of purified Ku and PARP to different sized dsDNA, we present a possible link for explaining the phenotypes. When compared with low LET IR at the same dose, high LET IR might induce similar yields of DNA DSBs in total but it might induce more small fragments of DNA DSBs (&lt;40 base pairs) that prevent Ku binding efficiently to two ends of one DSB fragment at the same time, thus delaying Ku-dependent repair. 

Retracted: No

PubPeer comments:
 Figure 4A. Much more similar than you would expect. https: imgur.com YIJMM0H , 
 Figure 6. Much more similar than you would expect. https: imgur.com uInCulO ,
SRSF6-regulated alternative splicing that promotes tumour progression offers a therapy target for colorectal cancer
Authors: Sunzhe Xie
Tianze Yu
Ledong Wan
Fengyan Han
Honghe Zhang
Wenjie Sun
Wenying Yu
Yihua Wu
Yuan Liu
Yuwei Zhou
Jianlu Kong
Enping Xu
Lei Zhang
Maode Lai
Enhui Shen
Journal: Gut (2019)
Discipline: CLINICAL MEDICINE
Keywords: SRSF6; alternative splicing; colorectal cancer; indacaterol.
Affiliations: Department of Pathology, Key Laboratory of Disease Proteomics of Zhejiang Province, School of Medicine, Zhejiang University, Hangzhou, China., State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China., College of Agriculture and Biotechnology, Institute of Bioinformatics, Zhejiang University, Hangzhou, China., Department of Toxicology, School of Public Health, Zhejiang University, Hangzhou, Zhejiang, China., Department of Pharmacology, China Pharmaceutical University, Nanjing, China.

Abstract:  Objective: To investigate the molecular function of splicing factor SRSF6 in colorectal cancer (CRC) progression and discover candidate chemicals for cancer therapy through targeting SRSF6. Design: We performed comprehensive analysis for the expression of SRSF6 in 311 CRC samples, The Cancer Genome Atlas and Gene Expression Omnibus (GEO) database. Functional analysis of SRSF6 in CRC was performed in vitro and in vivo. SRSF6-regulated alternative splicing (AS) and its binding motif were identified by next-generation RNA-sequencing and RNA immunoprecipitation sequencing (RIP-seq), which was validated by gel shift and minigene reporter assay. ZO-1 exon23 AS was investigated to mediate the function of SRSF6 in vitro and in vivo. Based on the analysis of domain-specific role, SRSF6-targeted inhibitor was discovered de novoby virtual screening in 4855 FDA-approved drugs and its antitumour effects were evaluated in vitroand in vivo. Results: SRSF6 was frequently upregulated in CRC samples and associated with poor prognosis, which promoted proliferation and metastasis in vitro and in vivo. We identified SRSF6-regulated AS targets and discovered the SRSF6 binding motif. Particularly, SRSF6 regulates ZO-1 aberrant splicing to function as an oncogene by binding directly to its motif in the exon23. Based on the result that SRSF6 RRM2 domain plays key roles in regulating AS and biological function, indacaterol, a Œ≤2-adrenergic receptor agonist approved for chronic obstructive pulmonary disease treatment, is identified as the inhibitor of SRSF6 to suppress CRC tumourigenicity. Conclusions: SRSF6 functions the important roles in mediating CRC progression through regulating AS, and indacaterol is repositioned as an antitumour drug through targeting SRSF6. Accession numbers: The accession numbers for sequencing data are SRP111763 and SRP111797. 

Retracted: No

PubPeer comments:
  , 
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Influence of Polymer Structure and Architecture on Drug Loading and Redox-Triggered Release
Authors: Peidong Wu
S Thayumanavan
Priyaa Prasad
Jingjing Gao
Pintu Kanjilal
Kingshuk Dutta
Journal: Biomacromolecules (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Disulfide cross-linked nanoassemblies; drug delivery vehicle; redox gradient; block copolymer; nanogels
Affiliations: Department of Chemistry, University of Massachusetts Amherst, Amherst, Massachusetts 01003, United States

Abstract:  Disulfide cross-linked nanoassemblies have attracted considerable attention as a drug delivery vehicle due to their responsiveness to the natural redox gradient in biology. Fundamentally understanding the factors that influence the drug loading capacity, encapsulation stability, and precise control of the liberation of encapsulated cargo would be profoundly beneficial to redox-responsive materials. Reported herein are block copolymer (BCP)-based self-cross-linked nanogels, which exhibit high drug loading capacity, high encapsulation stability, and controllable release kinetics. BCP nanogels show considerably higher loading capacity and better encapsulation stability than the random copolymer nanogels at micromolar glutathione concentrations. By partially substituting thiol-reactive pyridyl disulfide into the unreactive benzyl or butyl group, we observed opposite effects on the cross-linking process of BCP nanogels. We further studied the redox-responsive cytotoxicity of our drug-encapsulated nanogels in various cancer cell lines. 

Retracted: No

PubPeer comments:
 Figure S3, from the supplemental materials, was brought to my attention by a reader. * Blue boxes: Plots e and h look remarkably similar, although the symbols are different (e.g. the red dots in panel e look like the blue triangles in h). * Red boxes: Plots f and g look remarkably similar, although the symbols are different (e.g. the blue triangles dots in panel f look like the black squares in g).  , 
 Some of the bar plots shown in Figures 3, 7, S6, S7, and S9 appear to show unexpected irregularities * Cyan arrows: some error bars appear irregular, with crossbars of different widths, and the vertical line not always in the middle. * Pink arrows: Some lines at the top of the bar do not connect. There might be a perfectly good explanation for this, but could the authors please show the original measurements? Were these drawn by software or generated manually? As an example, here is Figure S6B:  , 
 In addition to the above comments, I also observed Fig 2C and Fig S2b black squares are identical.  ,
Effects of Omega-3 Fatty Acid Supplementation on Inflammatory Cytokines and Advanced Glycation End Products in Patients With Diabetic Nephropathy: a Randomized Controlled Trial
Authors: Seyyed Mehdi Mirhashemi
Faeze Rahimi
Alireza Soleimani
Zatollah Asemi
Journal: Iranian journal of kidney diseases (2016)
Discipline: CLINICAL MEDICINE
Keywords: omega-3 fatty acid; supplementation; inflammatory cytokines; advanced glycation end products; diabetic nephropathy
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran. .

Abstract:  Introduction: This study was performed to evaluate the effects of omega-3 fatty acid supplementation on inflammatory cytokines and advanced glycation end products (AGEs) in patients with diabetic nephropathy (DN). Materials and methods: This randomized double-blind placebo-controlled trial was done on 60 patients with DN who were randomly divided into 2 groups to receive either 1000 mg/d of omega-3 fatty acid from flaxseed oil (n = 30) or placebo (n = 30) for 12 weeks. The primary outcome variables were tumor necrosis factor-Œ±, receptor tumor necrosis factor-Œ± and growth differentiation factor 15. Fasting blood samples were taken at the onset and the end of the study to quantify the related markers. Results: Compared with the placebo, omega-3 fatty acid supplementation resulted in a significant decrease in serum AGEs (-2.3 ¬± 2.8 AU versus 0.2 ¬± 2.5 AU, P = .001). Despite a significant reduction in serum level of receptor for AGEs (-0.1 ¬± 0.3 AU, P = .02) in the omega-3 fatty acid group, no significant difference was found between the two groups in terms of their effects on the receptor for AGEs. Supplementation with omega-3 fatty acid had no significant effect on the inflammatory cytokines as compared with the placebo. Conclusions: Our study demonstrated that omega-3 fatty acid supplementation among DN patients had favorable effects on AGEs and the receptor for AGEs. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A67 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
A Novel Regulator of Preadipocyte Differentiation, Transcription Factor TCF21, Functions Partially Through Promoting LPL Expression
Authors: Hui Li
Chang Liu
Hui Zhang
Ning Wang
Yumao Li
Zhiping Cao
Bohan Cheng
Zhiqiang Du
Xinyang Zhang
Mengqi Wu
Journal: Frontiers in Physiology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: LPL; TCF21; chicken; differentiation; preadipocyte.
Affiliations: Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture and Rural Affairs, Harbin, China., Key Laboratory of Animal Genetics, Breeding and Reproduction, Education Department of Heilongjiang Province, Harbin, China., College of Animal Science and Technology, Northeast Agricultural University, Harbin, China.

Abstract:  The transcription factor TCF21 has been previously shown to be specifically expressed in white preadipocytes in mice. However, the exact biological function of TCF21 in the context of adipogenesis remains unknown. In the current study, we used chicken lines selected based on their abdominal fat content, and observed a significant decrease in TCF21 mRNA and protein levels in the abdominal fat of lean broilers relative to fat broilers. Moreover, TCF21 expression increased throughout preadipocyte differentiation in vitro. We also found that TCF21 knockdown and over-expression attenuated and promoted preadipocyte differentiation, respectively, as evidenced by appropriate changes in lipid droplet accumulation and altered expressions of C/EBPa, LPL, and A-FABP. Additional chromatin immunoprecipitation analyses and luciferase assays demonstrated that TCF21 promotes the transcription of LPL by directly binding to the E-box motif in the LPL promoter. Together, these results show that TCF21 is a novel regulator of preadipocyte differentiation, in part by directly promoting LPL expression. 

Retracted: No

PubPeer comments:
 I checked the Figure 3 to see the effects of knock-down of TCF21 by si-TCF21. Why didn t authors measure protein levels of TCF-21 after knock-down experiment? It looks like they performed western blots for over-expression experiment as shown in Figure 4. , 
 #1 Thank you for your comment on our article. For knock-down, si-TCF21 acts directly on the mRNA, resulting in the degradation of the mRNA level of TCF21, so we measured the mRNA levels of TCF21. For over-expression, we used a eukaryotic expression plasmid pCMV- HA-TCF21, it can express the HA-TCF21 fusion protein, so we measured protein levels of HA-TCF21. ,
The effect of Acupressure and Reiki application on Patient's pain and comfort level after laparoscopic cholecystectomy: A randomized controlled trial
Authors: Esra Anu≈ü Topdemir
Serdar Saritas
Journal: Complementary Therapies in Clinical Practice (2021)
Discipline: CLINICAL MEDICINE
Keywords: Acupressure; Comfort; Laparoscopic cholecystectomy; Pain; Reiki.
Affiliations: Atat√ºrk School of Health Sciences, Dicle University,Diyarbakƒ±r, Turkey. Electronic address: ., Department of Surgical Nursing, Faculty of Nursing, Inonu University, Malatya, Turkey. Electronic address: .

Abstract:  Background: The aim of the study was to examine the effect of Acupressure and Reiki application on patient's pain and comfort level after Laparoscopic cholecystectomy. Materials and methods: In this prospective, single blinded randomized controlled trial, subjects were 132 adult patients, hospitalized in the General Surgery clinics and underwent laparoscopic cholecystectomy of a Training and Research Hospital in Turkey. Subjects were then assigned including a Reiki group of 44 persons, an Acupressure group of 44 persons, and a control group of 44 persons. The pain and comfort levels of all the patients, before and after the Acupressure and Reiki treatments in the experimental group, and without any intervention in the control groups were determined at the 3rd postoperative hour, using Pain on Visual Analogue Scale (Pain on VAS), Perianesthesia Comfort Scale (PCS) and General Comfort Questionnaire (GCQ). The data analyses were performed using descriptive statistics, Shapiro Wilk test, paired samples t-test, Mann Whitney U test, ANOVA and LSD multiple comparison tests, Kruskal Wallis test and Wilcoxon test. Results: In the patients who received reiki and acupressure treatment, the pain level decreased, comfort level increased and the difference between the groups was found to be significant (p &lt; 0.05). Conclusion: Reiki and Acupressure applied to the patients after Laparoscopic cholecystectomy decreased the pain and increased the comfort level. 

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2021 05 21 oh-the-gallstones-a-journal-should-retract-a-paper-on-reiki-and-pain-says-a-critic for some comments. ,
The role of cordycepin in cancer treatment via induction or inhibition of apoptosis: implication of polyadenylation in a cell type specific manner
Authors: Hellinida Thomadaki
Andreas Scorilas
Maria Havredaki
Chris Milto Tsiapalis
Journal: Cancer Chemotherapy and Pharmacology (2007)
Discipline: CLINICAL MEDICINE
Keywords: anticancer drugs; apoptosis; cordycepin; polyadenylation; etoposide
Affiliations: Institute of Biology, NCSR Demokritos, Aghia Paraskevi Attikis, 15310 Athens, Greece.

Abstract:  Purpose: Most anticancer drugs show their antiproliferative and cytotoxic activity via induction of apoptosis. In the present study we assessed the implication and role of cordycepin, a polyadenylation-specific inhibitor and a well-known chemotherapeutic drug, in apoptosis, induced by the anticancer drug etoposide. Methods: For this purpose, a variety of leukemia and lymphoma cell lines (U937, K562, HL-60, Daudi, Molt-4) were treated with the anticancer drugs etoposide and/or cordycepin and assessed for poly(A) polymerase (PAP) activity and isoforms by the highly sensitive PAP activity assay and western blotting, respectively. Induction of apoptosis was determined by endonucleosomal DNA cleavage, DAPI staining, caspase-6 activity assay and DeltaPsi m reduction, whereas cytotoxicity and cell cycle status were assessed by Trypan blue staining, MTT assay and flow cytometry. Results and conclusions: The results showed that PAP changes in all cell lines, in response to apoptosis induced by etoposide, in many cases even prior to hallmarks of apoptosis (endonucleosomal cleavage of DNA, DeltaPsi(m) reduction). A further elucidation to this apoptosis-polyadenylation correlation was added, by cell treatment with cordycepin, resulting in either suppression (U937, K562) or induction (HL-60) of the apoptotic process, according to the cell type. However, inhibition of polyadenylation did not influence the cell lines Daudi and Molt-4 used, where alternative apoptotic pathways are induced through cleavage of DNA into high molecular weight fragments. 

Retracted: No

PubPeer comments:
null, 
 I was Peer 1. I reported this paper to the journal in June 2015, with a reminder in 2017, but no reply from the editors, and no action in the past five years. An additional finding in Figure 3A might be of interest as well. * Yellow boxes: the left 2 sample lanes appear to look very similar. Image made lighter to bring out details.  ,
Study of Anxiety/Depression in Patients with Coronary Heart Disease After Percutaneous Coronary Intervention
Authors: PeiYing Zhang
Journal: Cell Biochemistry and Biophysics (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Anxiety/depression; Coronary heart disease; Percutaneous coronary intervention.
Affiliations: Xuzhou Center Hospital, No.199 JieFang south Road, Xuzhou, 221009, Jiangsu, China. .

Abstract:  The objective of this study is to study the involvement of anxiety/depression in patients with coronary heart disease after percutaneous coronary intervention. Inpatients in the Department of Cardiology of Xuzhou Center Hospital from December 2012 to July 2014 were divided into stent group (100 cases) and the non-stent group (50 cases). Fifty cases in the stent group were treated with psychological methods, called intervention group, and other 50 cases were untreated and called non-intervention group. All patients were assessed for anxiety and depression using self-rating anxiety scale and self-rating depression scale, 1 day after admission, 1 day after coronary angiography, and when they were discharged. No significant differences were observed on biochemical criterion, and anxiety scores or depression scores between the stent and the non-stent groups before percutaneous coronary intervention (P value &gt;0.05 for all). After percutaneous coronary intervention, anxiety/depression scores in the intervention group and non-intervention group were significantly higher than those in the non-stent group (P &lt; 0.05). There were no significant differences between the intervention group and the non-intervention group on anxiety/depression scores (P &gt; 0.05). On the day of discharge, the anxiety/depression scores were the lowest in the intervention group (P &lt; 0.05). Coronary artery intervention can increase patients' anxiety/depression, but appropriate psychological intervention can reduce the negative emotions. 

Retracted: No

PubPeer comments:
  In this study, 150 inpatients with coronary artery disease in the Department of Cardiology of Xuzhou Center Hospital from December 2012 to July 2014 were studied. All the subjects underwent coronary angiography in the hospital. Patients were divided into two groups, stent group (100 cases), who received stent implantation during coronary angiography and the non-stent group (50 cases). According to Table 1, the two groups did not differ significantly in any health indicators.*  In the absence of any criteria for assigning people to the stent or non-stent groups, we are left to conclude that it was random. Were 50 patients deprived of presumably-beneficial treatment purely for the sake of a control group? -------------------------------------------------- * The legend of Table 1, and its contents, disagree about the presence of an Age comparison. ,
Impact of variable fluid properties on forced convection of Fe3O4/CNT/water hybrid nanofluid in a double-pipe mini-channel heat exchanger
Authors: Shahsavar, Amin
Godini, Ali
Sardari, Pouyan Talebizadeh
Toghraie, Davood
Salehipour, Hamzeh
Journal: Journal of Thermal Analysis and Calorimetry (2019)
Discipline: CHEMISTRY
Keywords: hydrothermal performance; non-Newtonian hybrid nanofluid; temperature-dependent; thermal conductivity; viscosity

Abstract: The objective of this study is to assess the hydrothermal performance of a non-Newtonian hybrid nanofluid with temperature-dependent thermal conductivity and viscosity compared with a Newtonian hybrid nanofluid with constant thermophysical properties. A counter-current double-pipe mini-channel heat exchanger is studied to analyze the effects of the hybrid nanofluid. The nanofluid is employed as the coolant in the tube side, while the hot water flows in the annulus side. Two different nanoparticles including tetramethylammonium hydroxide-coated Fe3O4 (magnetite) nanoparticles and gum arabic-coated carbon nanotubes are used to prepare the water-based hybrid nanofluid. The results demonstrated that the non-Newtonian hybrid nanofluid always has a higher heat transfer rate, overall heat transfer coefficient, and effectiveness than those of the Newtonian hybrid nanofluid, while the opposite is true for the pressure drop, pumping power, and performance evaluation criterion. Supposing that the Fe3O4-carbon nanotube/water hybrid nanofluid is a Newtonian fluid with constant thermal conductivity and viscosity, there leads to large error in the computation of pressure drop (1.5‚Ä?.71%), pumping power (1.5‚Ä?.71%), and performance evaluation criterion (18.24‚Ä?9.60%), whereas the errors in the computation of heat transfer rate, overall heat transfer coefficient, and effectiveness are not considerable (less than 2.91%).

Retracted: No

PubPeer comments:
 Please clarify if the basis for the developed models given in two papers, one in **2017** (Figures 12.b 13.b) and the other one in **2018** (Figures 2.a 2.b) shown below are the same. The other two papers in **2019** are self-referenced, but please clarify the strength of influence for the previously developed model applied in these newer works. There are also a few other items commented below. The first author (**Amin Shahsavar**) of the paper below published in **2016** is the common co-author in those papers, and wondering if the necessary and effective similarity checks were accordingly performed by the **journals editors!** Thanks.   ,
MiRNA-130a-3p inhibits cell proliferation, migration, and TMZ resistance in glioblastoma by targeting Sp1
Authors: Liang Han
Yao Fu
Zhaohui Li
Yu Tian
Zhijun Wang
Journal: American journal of translational research (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Specificity protein 1; TMZ resistance; glioblastoma; miR-130a-3p; proliferation.
Affiliations: Department of Neurosurgery, China-Japan Union Hospital of Jilin University Changchun 130033, P. R. China., Department of Pediatric Surgery, The First Hospital of Jilin University Changchun 130000, P. R. China., Department of Pathology, China-Japan Union Hospital of Jilin University Changchun 130033, P. R. China.

Abstract:  Specificity protein 1 (Sp1) is aberrantly expressed and involved in the development and metastasis of glioblastoma. In this study, we observed that the expression of Sp1 was upregulated while that of microRNA (miR)-130a-3p was downregulated in glioblastoma cell lines. Sp1 was validated as a target of miR-130a-3p; increased levels of miR-130a-3p inhibited the proliferation, migration, and temozolomide (TMZ) resistance of the glioblastoma cells. However, Sp1 overexpression compromised the inhibitory effects of miR-130a-3p. Our study elucidates the functional interaction between miR-130a-3p and Sp1 in the development and progression of glioblastoma, suggesting a potential therapeutic target for the disease. 

Retracted: No

PubPeer comments:
 The flow cytometry images seem, in many places, to be stitched together from multiple plots, or possibly be re-gatings of the same data. There are far too many plots in the paper, so I have opted to show only four panels from one of the figures below.  ,
Physcion 8-O-Œ≤-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/STAT3 signalling
Authors: Qiuming Li
Yong Lv
Weiwei Wan
Guangming Wan
Xuemin Jin
Fengyan Zhang
Wencui Wan
Yang Long
Journal: Artificial Cells Nanomedicine and Biotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Diabetic retinopathy; NORAD; STAT3; miR-125; physcion 8-O-Œ≤-glucopyranoside.
Affiliations: Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Abstract:  Diabetic retinopathy (DR) is the leading cause of decreased vision and blindness globally. The aim of this study was to understand the role of physcion 8-O-Œ≤-glucopyranoside (PG) in high glucose (HG)-induced DR and to investigate whether lncRNA NORAD/miR-125/STAT3 signalling was the underlying mechanism involved in DR. To this end, the serum levels of NORAD, miR-125, and STAT3 were determined in patients with DR. The APRE-19 cells were subjected to HG treatment to construct the cell model of DR. HG-disposed APRE-19 cell injury was assessed by detecting cell viability, apoptosis, concentrations of pro-inflammatory cytokines including TNF-Œ± and IL-1Œ≤, and ROS generation. Moreover, the effect of PG on HG-disposed APRE-19 cell injury was investigated. NORAD was then overexpressed to investigate the combined effects of NORAD overexpression and PG on HG-disposed APRE-19 cell injury. Furthermore, the regulatory relationship between NORAD and miR-125 as well as miR-125 and STAT3 was investigated. The expression levels of NORAD and STAT3 were significantly increased in the serum of DR patients, while the miR-125 expression was decreased. The HG treatment-induced injury to APRE-19 cells, which were alleviated by PG treatment. Moreover, PG alleviated HG-disposed injury to ARPE-19 cells by decreasing NORAD. NORAD negatively regulated miR-125 expression and the combined effects of NORAD and PG on HG-disposed ARPE-19 cell injury were reversed by miR-125 overexpression. Furthermore, STAT3 was confirmed as a target gene of miR-125. Our results show that PG exerts protective roles in HG-disposed DR via regulating lncRNA NORAD/miR-125/STAT3 signalling. NORAD/miR-125/STAT3 axis may provide a novel perspective for target therapy of DR. 

Retracted: No

PubPeer comments:
 In Figure 4B, part of a flow cytometry dot plot has been duplicated and presented as something else (modified).  , 
 #1 More color-coded panels in Fig 4B:  For comparison with Fig 6A of [Zhu et al (2018)]  Fig 3C of [Wang et al (2019)]  Many other sightings noted in those threads. , 
 Fig4A.  , 
 Fig 5A.  Some details highlighted for comparison with Figures 5A of [Guo et al (2018)]  4A of [Li et al (2017)]  Fig 6 (TPC-1 section) of [Zhao et al (2016)]  Many other sightings in those threads. ,
Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells
Authors: Warren Fiskus
Veena Coothankandaswamy
Eduardo Sotomayor
Andrew Savoie
Kathleen M Buckley
Kyungsoo Ha
Atul Joshi
Rekha Rao
Peter Atadja
Jianguo Tao
Srilatha Nalluri
Kapil N Bhalla
Ramesh Balusu
Journal: Clinical Cancer Research (2010)
Discipline: CLINICAL MEDICINE
Keywords: Bortezomib; Panobinostat; Unfolded protein response; Endoplasmic reticulum stress; MCL cells
Affiliations: The University of Kansas Cancer Center, Kansas City, 66160, USA.

Abstract:  Purpose: Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL). Here, we determined the molecular basis of the improved in vitro and in vivo activity of the combination of the pan-histone deacetylase inhibitor panobinostat and bortezomib against human, cultured, and primary MCL cells. Experimental design: Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells. Results: Treatment with panobinostat induced heat shock protein 90 acetylation; depleted the levels of heat shock protein 90 client proteins, cyclin-dependent kinase 4, c-RAF, and AKT; and abrogated bortezomib-induced aggresome formation in MCL cells. Panobinostat also induced lethal UPR, associated with induction of CAAT/enhancer binding protein homologous protein (CHOP). Conversely, knockdown of CHOP attenuated panobinostat-induced cell death of MCL cells. Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells. Cotreatment with panobinostat also increased bortezomib-mediated in vivo tumor growth inhibition and improved survival of mice bearing human Z138C MCL cell xenograft. Conclusion: These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib. 

Retracted: No

PubPeer comments:
  , 
 2020 editor s note. https: clincancerres.aacrjournals.org content 26 6 1531 The editors are publishing this note to alert readers to a concern about this article (1): splice lines are missing between lanes 1 and 2 in both Figs. 1B (acetyl lysine lane at 48 hours) and 3D. , 
 In Figure 3D and Figure 1B of the manuscript (10.1158 1078-0432.CCR-10-0529), the immunoblot data shown were generated in the same experiment, and cell lysates were run on the same gels. However, we did not include data from all experimental conditions in the immunoblots presented. It was an oversight that a vertical splice line was not placed between 0 and 50 nmol L of panobinostat (Figure 3D) and between the control and siHDAC6 lanes (figure 1B), to indicate repositioned gel images. , 
 #3 Are the uncropped scans still available? ,
Comparison of myo-inositol and metformin¬†on clinical, metabolic and genetic parameters in polycystic ovary syndrome: A randomized controlled clinical trial
Authors: Mehri Jamilian
Faraneh Afshar Ebrahimi
Zatollah Asemi
Hamidreza Jamilian
Pegah Farhat
Esmat Aghadavod
Bita Badehnoosh
Fereshteh Bahmani
Fatemeh Foroozanfard
Journal: Clinical Endocrinology (2017)
Discipline: CLINICAL MEDICINE
Keywords: hormonal status; inflammation; metformin; myo-inositol; oxidative stress
Affiliations: Endocrinology and Metabolism Research Center; Arak University of Medical Sciences; Arak Iran, Department of Gynecology and Obstetrics; School of Medicine; Kashan University of Medical Sciences; Kashan Iran, Research Center for Biochemistry and Nutrition in Metabolic Diseases; Kashan University of Medical Sciences; Kashan Iran, Department of Gynecology and Obstetrics; School of Medicine; Alborz University of Medical Sciences; Karaj Iran, Department of Psychiatry; Arak University of Medical Sciences; Arak Iran

Abstract:  Objective: To our knowledge, data on comparison of myo-inositol and metformin on clinical, metabolic and genetic parameters in subjects with polycystic ovary syndrome (PCOS) are limited. This study was carried out to compare myo-inositol and metformin on clinical, metabolic and genetic parameters in subjects with PCOS. Design, patients and measurements: This randomized controlled trial was conducted among 60 subjects with PCOS aged 18-40 years. Subjects were randomly allocated into two groups to receive either myo-inositol (N=30) or metformin (N=30) for 12 weeks. Gene expression of inflammatory cytokines was assessed in peripheral blood mononuclear cells (PBMCs) of PCOS women by RT-PCR. Results: After the 12-week intervention, compared with metformin, myo-inositol intake significantly decreased serum total testosterone (-1.4¬±4.2 vs +0.7¬±1.4 nmol/L, P=.03), modified Ferriman-Gallwey (mF-G) scores (-1.1¬±0.7 vs -0.5¬±0.8, P=.01) and serum high-sensitivity C-reactive protein (hs-CRP) levels (-2.6¬±3.9 vs +0.2¬±1.5 mg/L, P&lt;.001). RT-PCR demonstrated that compared with metformin, myo-inositol downregulated gene expression of interleukin-1 (IL-1) (P=.02) in PBMCs of subjects with PCOS. We did not observe any significant effect of myo-inositol intake compared with metformin on other hormonal profiles, plasma nitric oxide (NO) or gene expression of IL-8 and tumour necrosis factor alpha (TNF-Œ±). Conclusions: Overall, taking myo-inositol, compared with metformin, for 12 weeks in patients with PCOS with hyperinsulinism and normoinsulinism had beneficial effects on total testosterone, mFG scores, serum hs-CRP levels and gene expression of IL-1, but did not affect other hormonal profiles, NO levels or gene expression of IL-8 and TNF-Œ±. 

Retracted: No

PubPeer comments:
 A very very unusual ranking method is used in Table 2.  ,
Retracted: Cypermethrin exposure leads to regulation of proteins expression involved in neoplastic transformation in mouse skin
Authors: Jasmine George
Amit Kumar Srivastava
Yogeshwer Shukla
Richa Singh
Journal: PROTEOMICS (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cypermethrin; carcinogenic effects; protein expression; neoplastic transformation; mouse skin
Affiliations: Proteomics Laboratory, CSIR‚ÄêIndian Institute of Toxicology Research, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, India

Abstract:  Cypermethrin, a synthetic pyrethroid insecticide is shown to exert carcinogenic effects in rodents; however, its underlying mechanism remains elusive. Here, we showed the effect of cypermethrin on protein expression involved in neoplastic transformation in mouse skin. Comparative protein expression profiles between untreated control and cypermethrin-treated mouse skin were explored using 2-DE. A total of 27 spots that were statistically significant (p&lt;0.05) and differentially expressed in response to cypermethrin exposure were identified by MALDI-TOF/TOF and LC-MS/MS. Among them, six up-regulated proteins (carbonic anhydrase 3 (Ca 3), Hsp-27, S100A6, galectin-7, S100A9, S100A11) and one down-regulated protein (superoxide dismutase [Cu-Zn] (Sod 1)) are associated with cancer-related key processes. These selected dysregulated proteins were further validated in 2-DE gels of mouse skin treated with known tumorigens (benzo-[a]-pyrene, 12-O-tetradecanoyl-phorbol-13-acetate and mezerein), respectively. Comparative studies showed that Ca 3, S100A6, S100A9, S100A11 and Sod 1 are specific for stages of development and progression of tumors whereas Hsp-27 and galectin-7 are specific for tumor promotion stage by cypermethrin in mouse skin. Furthermore, these chosen proteins confirmed by Western blotting and immunofluorescence staining were consistent with changes in 2-DE check. This proteomic investigation for the first time provides key proteins that will contribute in understanding the mechanism behind cypermethrin-induced neoplastic transformation. 

Retracted: No

PubPeer comments:
 It appears to readers on social media that the backgrounds atop and below most of the actin stains may have been removed. Could the authors provide the uncropped original scan to reassure readers? ***  , 
 November 2, 2020 u201cThe Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates.u201d ,
Protective Properties and Surface Localization of Plasmodium falciparum Enolase
Authors: Shobhona Sharma
Monika Mehta
Ipsita Pal-Bhowmick
Isabelle Coppens
Gotam K Jarori
Journal: Infection and Immunity (2007)
Discipline: IMMUNOLOGY
Keywords: enolase; Plasmodium falciparum; antigenic properties; cell wall; Candida albicans
Affiliations: Department of Biological Sciences, TIFR, Homi Babha Road, Colaba, Mumbai 400 005, India., Department of Biological Sciences, Tata Institute of Fundamental Research, Homi Bhabha Road, Colaba, Mumbai 400 005, India, Johns Hopkins Bloomberg School of Public Health, Malaria Research Institute, Baltimore, Maryland

Abstract:  The enolase protein of the human malarial parasite Plasmodium falciparum has recently been characterized. Apart from its glycolytic function, enolase has also been shown to possess antigenic properties and to be present on the cell wall of certain invasive organisms, such as Candida albicans. In order to assess whether enolase of P. falciparum is also antigenic, sera from residents of a region of Eastern India where malaria is endemic were tested against the recombinant P. falciparum enolase (r-Pfen) protein. About 96% of immune adult sera samples reacted with r-Pfen over and above the seronegative controls. Rabbit anti-r-Pfen antibodies inhibited the growth of in vitro cultures of P. falciparum. Mice immunized with r-Pfen showed protection against a challenge with the 17XL lethal strain of the mouse malarial parasite Plasmodium yoelii. The antibodies raised against r-Pfen were specific for Plasmodium and did not react to the host tissues. Immunofluorescence as well as electron microscopic examinations revealed localization of the enolase protein on the merozoite cell surface. These observations establish malaria enolase to be a potential protective antigen. 

Retracted: No

PubPeer comments:
   Image recycling between two papers. ,