PReD-Bench/PRed-Bench huggingface dataset:
Resveratrol protects the integrity of alveolar epithelial barrier via SIRT1/PTEN/p‐Akt pathway in methamphetamine‐induced chronic lung injury
Authors: Ming Liu
Yun Wang
Lei Chen
Ashok Kumar
Lian Liu
Xin Wang
Ming-Yuan Zhou
Lin Cheng
Lin Shi
Ying-Jian Gu
Mei-Jia Zhu
Yuan-Ling Zhao
Journal: Cell Proliferation (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PTEN; SIRT1; alveolar epithelial cells; apoptosis; methamphetamine
Affiliations: Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China., Department of Drug Control, Criminal Investigation Police, University of China, Shenyang, China., Department of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, TX, USA.

Abstract:  Objectives: SIRT1 is an antioxidative factor, but its mechanism in methamphetamine (MA)-induced lung injury remains unclear. The purpose of this study is to determine whether MA can disrupt the integrity of alveolar epithelial barrier, whether SIRT1 is involved in MA-induced chronic lung injury and whether Resveratrol (Res) can protect the integrity of alveolar epithelial cells by regulating ROS to activate SIRT1/PTEN/p-Akt pathway. Materials and methods: The rats were randomly divided into control group and MA group. Extracted lungs were detected by Western blot, HE staining and immunohistochemistry. The alveolar epithelial cells were treated with MA or/and Res, following by Western blot, LDH leakage assay and flow cytometry. MOE is used for bio-informatics prediction. Results: Chronic exposure to MA can cause slower growth ratio of weight, increased RVI and induced lung injury including the reduced number of alveolar sacs and the thickened alveolar walls. MA-induced apoptosis was associated with SIRT1-related oxidative stress. Res suppressed ROS levels, activated SIRT1, negatively regulated PTEN, phosphorylated Akt, reduced LDH leakage, increased the expression of ZO-1 and E-cadherin and inhibited the apoptosis of alveolar epithelial cells to attenuate MA-induced higher permeability of alveolar epithelium. Conclusions: MA disrupted the integrity of alveolar epithelial barrier. Res inhibited oxidative stress and reversed MA-induced higher permeability and apoptosis of alveolar epithelium by the activation of SIRT1/PTEN/p-Akt pathway. 

Retracted: No

PubPeer comments:
 Figure 3F. * Blue boxes: In the 6h row, two panels depicting two different concentrations appear to look the same. ![file] ,
Ginseng and Its Active Components Ginsenosides Inhibit Adipogenesis in 3T3-L1 Cells by Regulating MMP-2 and MMP-9
Authors: Dongmin Park
Michung Yoon
Jaeho Oh
Jiwon Ahn
Soon Shik Shin
Hyunghee Lee
Journal: Evidence-based Complementary and Alternative Medicine (2012)
Discipline: CLINICAL MEDICINE
Keywords: adipogenesis; angiogenesis; extracellular matrix remodeling; ginseng; ginsenosides
Affiliations: Department of Life Sciences, Mokwon University, Daejeon 302-729, Republic of Korea., Department of Life Sciences, Mokwon University, Daejeon 302-729, Republic of Korea, Genome Research Center, KRIBB, Daejeon 305-806, Republic of Korea, Department of Formula Sciences, College of Oriental Medicine, Dong-Eui University, Busan 614-052, Republic of Korea

Abstract:  The growth and development of adipose tissue are believed to require adipogenesis, angiogenesis, and extracellular matrix remodeling. As our previous study revealed that ginseng reduces adipose tissue mass in part by decreasing matrix metalloproteinase (MMP) activity in obese mice, we hypothesized that adipogenesis can be inhibited by ginseng and its active components ginsenosides (GSs). Treatment of 3T3-L1 adipocytes with Korean red ginseng extract (GE) inhibited lipid accumulation and the expression of adipocyte-specific genes (PPARγ, C/EBPα, aP2, and leptin). GE decreased both the mRNA levels and activity of MMP-2 and MMP-9 in 3T3-L1 cells. These effects were further inhibited by total GSs (TGSs) and individual GSs. TGSs and individual GSs also significantly decreased MMP-2 and MMP-9 reporter gene activities in the presence of phorbol 12-myristate 13-acetate (PMA), the MMP inducer. Among the GSs, Rb1 most effectively inhibited MMP activity. In addition, PMA treatment attenuated the inhibitory actions of GE and GSs on adipogenesis. Moreover, GE and GSs reduced the expression of NF-κB and AP-1, the transcription factors of MMP-2 and MMP-9. These results demonstrate that ginseng, in particular GSs, effectively inhibits adipogenesis and that this process may be mediated in part through the suppression of MMP-2 and MMP-9. Thus, ginseng and GSs likely have therapeutic potential for controlling adipogenesis. 

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. ,
FNDC4 Inhibits RANKL-Induced Osteoclast Formation by Suppressing NF-κB Activation and CXCL10 Expression
Authors: An-Min Chen
Shuang Liang
Kun Chen
Jia-Ming Zhang
Peng Cheng
Hui Liao
Jia-Chao Guo
Zheng-Tao Lv
Qing Yang
Chen-He Zhou
Journal: BioMed Research International (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: FNDC4; osteoclast formation; inflammation; macrophages; colitis
Affiliations: Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China, Department of Orthopedic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Abstract:  FNDC4 acts as an anti-inflammatory factor on macrophages and improves mouse model of induced colitis. Considering osteoclast formation is characterized by the activation of inflammation-related pathways, we thus speculated that FNDC4 may play a pivotal role in this process. RT-qPCR analysis was performed to confirm the expression of osteoclast formation related genes in primary murine bone marrow macrophages (BMMs). RANKL-treated BMMs were cultured with FNDC4 to evaluate the effect of FNDC4 on osteoclast differentiation. TRAP staining and bone resorption pits assay were used to assess osteoclast formation and bone resorption, respectively. Luciferase assay and western blotting analysis were conducted to determine whether FNDC4 inhibited osteoclast formation via NF-κB signaling in RAW 264.7 cells. Furthermore, to identify gene signatures in FNDC4-treated BMMs and to use these to elucidate the underlying molecular mechanisms during osteoclast formation, we adopted a bioinformatics approach by downloading the GSE76172 gene expression profiling dataset from the Gene Expression Omnibus (GEO) database. FNDC4 inhibited RANKL-induced osteoclastogenesis and mature osteoclast resorptive function in a dose-dependent manner. Results of NF-κB luciferase assay suggested that FNDC4 could significantly suppress the RANKL-induced NF-κB transcriptional activity. Based on the protein-protein interaction network, CXCL10 was identified as the differentially expressed gene with the highest connectivity degree (degree = 23); it was drastically downregulated in the presence of FNDC4, but supplementation of CXCL10 (10 ng/mL) partially ameliorated the FNDC4-induced inhibition of osteoclast formation. Taken together, we speculated that FNDC4 could suppress osteoclast formation via NF-κB pathway and downregulation of CXCL10. 

Retracted: No

PubPeer comments:
 ![file] ,
Development of self-assembled nanoceramic carrier construct(s) for vaccine delivery
Authors: Rishi Paliwal
Amit K Goyal
Neeraj Mishra
Shailja Tiwari
Shivani Paliwal
Suresh P Vyas
Bhuvaneshwar Vaidya
Kapil Khatri
Abhinav Mehta
Journal: Journal of biomaterials applications (2009)
Discipline: CLINICAL MEDICINE
Keywords: Hydroxyapatite; nanoceramic; immunoadjuvant; MSP-1(19); antigen
Affiliations: Department of Pharmaceutical Sciences, Drug Delivery Research Laboratory, Dr Harisingh Gour Vishwavidyalaya, Sagar (MP) 470003, India.

Abstract:  Hydroxyapatite (HA) has been extensively investigated as scaffolds for tissue engineering, as drug delivery agents, as non-viral gene carriers, as prosthetic coatings, and composites. Recent studies in our laboratory demonstrated the immunoadjuvant properties of HA when administered with malarial merozoite surface protein-1(19) (MSP-1(19)). HA nanoceramic carrier was prepared by co-precipitation method that comprises of sintering and spray-drying technique. Prepared systems were characterized for crystallinity, size, shape, and antigen loading efficiency. Small size and large surface area of prepared HA demonstrated good adsorption efficiency of immunogens. Prepared nanoceramic formulations also showed slower in vitro antigen release and slower biodegrability behavior, which may lead to a prolonged exposure to antigen-presenting cells and lymphocytes. Furthermore, addition of mannose in nanoceramic formulation may additionally lead to increased stability and immunological reactions. Immunization with MSP-1(19) in nanoceramic-based adjuvant systems induced a vigorous immunoglobulin G (IgG) response, with higher IgG2a than IgG1 titers. In addition considerable amount of IFN-g and IL-2 was observed in spleen cells of mice immunized with nanoceramic-based vaccines. On the contrary, mice immunized with MSP-1(19) alone or with alum did not exhibit a significant cytotoxic response. The antibody responses to vaccine co-administered with HA was a mixed Th1/Th2 compared to the Th2-biased response obtained with alum. The prepared HA nanoparticles exhibit physicochemical properties that appear promising to make them a suitable immunoadjuvant to be used as antigen carriers for immunopotentiation. 

Retracted: No

PubPeer comments:
 Fig 1.  Characterization of prepared HA:...(b) TEM image of prepared ceramic decoy with MSP-119 (i) **HA (without spray dried)**, (ii) HAS (spray dried); (c) XRD analysis of spraydried Ha; (d) EDAX analysis of spray-dried HA. ![file] Fig 1A from [Goyal et al (2008)] :  Electron microphotograph of different formulations: **(A) transmission electron microscope (TEM) image plain hydroxyapatite**; (B) TEM image of cellobiose-coated aquasomes; (C) TEM image of trehalose-coated aquasomes. ![file] It is unclear whether the marked panel represents particles of plain pulvverised hydroxyapatite, or of hyoxyapatite synthesised without spray-drying and then coated with MSP-119. ,
Microbiota, a New Playground for the Omega-3 Polyunsaturated Fatty Acids in Cardiovascular Diseases
Authors: Guy Rousseau
Journal: Marine Drugs (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Omega-3 PUFA; cardiovascular diseases; dysbiosis; microbiota.
Affiliations: Centre de Biomédecine, Hôpital du Sacré-Cœur, CIUSSS du Nord de l'île de Montréal, 5400 boul. Gouin Ouest, Montréal, QC H4J 1C5, Canada., Département de Pharmacologie et de Physiologie, Université de Montréal, Montréal, QC H3T 1J4, Canada.

Abstract:  Several cardioprotective mechanisms attributed to Omega-3 polyunsaturated fatty acids (PUFAs) have been studied and widely documented. However, in recent years, studies have supported the concept that the intestinal microbiota can play a much larger role than we had anticipated. Microbiota could contribute to several pathologies, including cardiovascular diseases. Indeed, an imbalance in the microbiota has often been reported in patients with cardiovascular disease and produces low-level inflammation. This inflammation contributes to, more or less, long-term development of cardiovascular diseases. It can also worsen the symptoms and the consequences of these pathologies. According to some studies, omega-3 PUFAs in the diet could restore this imbalance and mitigate its harmful effects on cardiovascular diseases. Many mechanisms are involved and included: (1) a reduction of bacteria producing trimethylamine (TMA); (2) an increase in bacteria producing butyrate, which has anti-inflammatory properties; and (3) a decrease in the production of pro-inflammatory cytokines. Additionally, omega-3 PUFAs would help maintain better integrity in the intestinal barrier, thereby preventing the translocation of intestinal contents into circulation. This review will summarize the effects of omega-3 PUFAs on gut micro-biota and the potential impact on cardiac health. 

Retracted: No

PubPeer comments:
 This paper proposes that the so called  leaky gut syndrome could be behind various cardiovascular diseases. Leaky Gut Syndrome is a condition that has little scientific evidence backing up its existence and several papers have been published disputing its existence and purported treatment. https: pubmed.ncbi.nlm.nih.gov 26760399 https: www.ncbi.nlm.nih.gov pmc articles PMC3758766 - Thus, the leaky gut cures being sold at a variety of internet sites and alternative medicine stores should be considered with caution. None have been tested in randomized clinical trials, and they may do more harm than good. ,
A double-blind comparison of the efficacy and safety of lorazepam and diazepam in the treatment of the acute alcohol withdrawal syndrome
Authors: L McCurdy
W C Miller Jr
Journal: Clinical Therapeutics (1984)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lorazepam; diazepam; acute alcohol withdrawal syndrome; efficacy; safety

Abstract:  The safety and efficacy of lorazepam and diazepam were compared in the treatment of the acute alcohol withdrawal syndrome during a five-day double-blind trial in alcoholic patients. The daily doses of lorazepam and diazepam were tapered from 6 or 8 mg to 2 mg and from 30 or 40 mg to 10 mg, respectively, during the first four days; no medication was given on day 5. Drug efficacy was measured by Total Severity Assessment Scores (TSAS), the three TSAS factor scores, and by the physician's global evaluation. Of the 55 inpatients enrolled, 47 completed the study. There were no statistically significant differences between the treatment groups in any of the efficacy assessment measures. The physical conditions of the majority of the patients treated with lorazepam (57%) and diazepam (59%) improved during therapy. There were no clinically significant differences between the treatment groups in vital signs or laboratory values. The results of this study indicate that lorazepam is as effective as diazepam in reducing the symptoms of acute alcohol withdrawal. When lorazepam and diazepam are compared in terms of their pharmacokinetics, lorazepam may have therapeutic advantages for the management of the acute alcohol withdrawal syndrome. 

Retracted: No

PubPeer comments:
 This article argues for the use of lorazepam over diazepam for the treatment of alcohol withdrawal. However I have discovered several concerning issues with this manuscript. 1) Multiple regions of text exactly the same in the following publications: Miller WC Jr, McCurdy L. A double-blind comparison of the efficacy and safety of lorazepam and diazepam in the treatment of the acute alcohol withdrawal syndrome. Clin Ther. 1984;6(3):364-71. PMID: 6722863. O Brien, J. E., Meyer, R. E., Thoms, D. C. (1983). Double-blind comparison of lorazepam and diazepam in the treatment of the acute alcohol abstinence syndrome. Current Therapeutic Research - Clinical and Experimental, 34(5), 825-831. 2) There are undisclosed conflicts of interest with Wyeth LLC, the original developer of lorazepam. These conflicts are also present in the two publications (above) that share identical text with this article. ,
Trichostatin A alleviates the process of breast carcinoma by downregulating LPAR5
Authors: Y-J Zhang
X-R Li
X Miao
M-F Hu
Y-Q Zheng
J Li
Y-S Zhu
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Histone deacetylase inhibitor; Trichostatin A; metastasis; breast carcinoma; LPAR5
Affiliations: Department of General Surgery, First Medical Center, PLA General Hospital, Beijing, China. .

Abstract:  Objective: To elucidate the role of histone deacetylase inhibitor Trichostatin A (TSA) in affecting metastasis of breast carcinoma, and its molecular mechanism. Patients and methods: LPAR5 levels in breast carcinoma tissues and paracancerous tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and its expression pattern was further verified in breast carcinoma cell lines. The relationship between LPAR5 and prognosis of breast carcinoma patients was analyzed. After TSA induction (100-400 nmol/L) for 6-48 h, the proliferative and migratory abilities of SKBR3 and MDA-MB-231 cells in overexpressing LPAR5 were examined by cell counting kit-8 (CCK-8), transwell and wound healing assay. By constructing a xenograft model in nude mice, the influences of TSA and LPAR5 on in vivo growth of breast carcinoma were examined. Results: LPAR5 was upregulated in breast carcinoma samples. High level of LPAR5 predicted higher rates of lymphatic metastasis and distant metastasis, as well as lower overall survival and progression-free survival in breast carcinoma patients. LPAR5 level was dose-dependently downregulated in TSA-induced SKBR3 and MDA-MB-231 cells. In addition, TSA induction dose-dependently declined proliferative ability, and time-dependently attenuated migratory ability in breast carcinoma cells. In vivo overexpression of LPAR5 in nude mice reversed the inhibitory effect of TSA on breast carcinoma growth. Conclusions: TSA induction can suppress proliferative and migratory abilities in breast carcinoma by downregulating LPAR5. 

Retracted: No

PubPeer comments:
 Fig 1.  D, Overall survival in breast carcinoma patients based on LPAR5 expression; E, Progression-free survival in breast carcinoma patients based on LPAR5 expression . ![file] The two K-M curves for the high-LPAR5 group are identical for the last 20 months, implying that those patients died in the same month that they relapsed. For the low-LPAR5 group, sometimes the overall survival curve is higher, sometimes the progression-free curve... some people relapsed and then died; some died and then relapsed. ![file] ,
A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants
Authors: Gary Ruvkun
Christian G Riedel
Xiaoyun Wu
Sean P Curran
Journal: Nature (2009)
Discipline: Multidisciplinary
Keywords: germ line; genomic instability; somatic maintenance; Caenorhabditis elegans; longevity
Affiliations: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.

Abstract:  Unlike the soma, which ages during the lifespan of multicellular organisms, the germ line traces an essentially immortal lineage. Genomic instability in somatic cells increases with age, and this decline in somatic maintenance might be regulated to facilitate resource reallocation towards reproduction at the expense of cellular senescence. Here we show that Caenorhabditis elegans mutants with increased longevity exhibit a soma-to-germline transformation of gene expression programs normally limited to the germ line. Decreased insulin-like signalling causes the somatic misexpression of the germline-limited pie-1 and pgl family of genes in intestinal and ectodermal tissues. The forkhead boxO1A (FOXO) transcription factor DAF-16, the major transcriptional effector of insulin-like signalling, regulates pie-1 expression by directly binding to the pie-1 promoter. The somatic tissues of insulin-like mutants are more germline-like and protected from genotoxic stress. Gene inactivation of components of the cytosolic chaperonin complex that induce increased longevity also causes somatic misexpression of PGL-1. These results indicate that the acquisition of germline characteristics by the somatic cells of C. elegans mutants with increased longevity contributes to their increased health and survival. 

Retracted: No

PubPeer comments:
 Another recent publication u201cActivation of DAF-16 FOXO by reactive oxygen species comtributes to longevity in long-lived mitochondrial mutants in Caenorhabditis elegansu201d ; doi: 10.1371 journal.pgen.1007268 also fails to observe alterations on pgl-1 3 expression in daf-2 mutants. Actually, their data suggest a downregulation of pgl-1 and pgl-3 compared to wild-type worms. Could authors kindly comment if they were capable of reproducing the data published in this papers? If not, shouldnu2019t they consider a correction? It seems that the central message of the paper is that germline genes are expressed in the somatic tissues of daf-2 mutants, and this is a mechanism of lifespan extension, but other groups canu2019t replicate these central findings. , 
 Could authors please clarify why so many animals presented a roller phenotype on Supplementary Fig. 8? WT and daf-2(e1368) mutants shouldn t present this phenotype ![file] , 
 Data from this paper could not be reproduced by Knutson et al., 2016 (doi: 10.1073 pnas.1523402113) In their hands: (i) daf-2 mutant worms don t express germ-line proteins or transcripts in their somatic cells; (ii) RNAi for pgl-1, -3, glh-1, glh-4, mes-4 didn t decrease daf-2 lifespan Can the authors comment if they tried to replicate their findings or if they will proceed with a correction? ,
Mercury assisted fluorescent supramolecular assembly of hexaphenylbenzene derivative for femtogram detection of picric acid
Authors: Subhamay Pramanik
Vandana Bhalla
Manoj Kumar
Journal: Analytica Chimica Acta (2013)
Discipline: CHEMISTRY
Keywords: AIEE; Femtogram level detection of PA; Hexaphenylbenzene; Hg(2+) chemosensor; Self assembled nanofibres.
Affiliations: Department of Chemistry, UGC Sponsored Centre for Advanced Studies-1 Guru Nanak Dev University, Amritsar 143005, Punjab, India.

Abstract:  Aggregates of hexaphenylbenzene derivatives 3, having pyrene groups form network of fluorescent nanofibres in presence of mercury ions. Further, fluorescent nanofibres of 3-Hg(2+) supramolecular ensemble exhibit sensitive and pronounced response towards the picric acid. In addition, the solution coated paper strips of 3-Hg(2+) supramolecular ensemble can detect picric acid in the range of 2.29 fg/cm(2), thus, providing a simple, portable and low cost method for detection of picric acid in solution and in contact mode. 

Retracted: No

PubPeer comments:
 Figure 5 and 9, all the spectra appear to have the same noise. ![file] ![file] , 
 Some of the spectra in figure 11 as well: ![file] , 
 From several of the Supporting Information figures, like Fig. S3, that have similarly identical noiseu2026 one could probably extract raw data (Excel) to confirm. ,
Blockade of AP1 transactivation abrogates the abnormal expression of breast cancer-specific gene 1 in breast cancer cells
Authors: AiPing Lu
Jingwen Liu
Fang Zhang
Anu Gupta
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: BCSG1; breast cancer; gene expression; AP1; transcription factors
Affiliations: Department of Veterans Affairs, Palo Alto Health Care System, Palo Alto, California 94304, USA.

Abstract:  Breast cancer-specific gene 1 (BCSG1) is not expressed in normal breast tissue but is highly expressed in the vast majority of invasive and metastatic breast carcinomas. When over-expressed, BCSG1 significantly stimulates the proliferation and invasion of breast cancer cells. The accumulated evidence suggests that the aberrant expression of BCSG1 in breast carcinomas is caused by transcriptional activation of the BCSG1 gene. However, the transcription factors that activate BCSG1 transcription have not been identified. In this study, we extensively investigated the role of AP1 in BCSG1 expression in breast cancer cells. We demonstrate that there are two closely located AP1 binding sites residing in the first intron of the BCSG1 gene. Mutation of either AP1 motif on the BCSG1 promoter constructs markedly reduces the promoter activity. We further show that 12-O-tetradecanoylphorbol-13-acetate (TPA) increases BCSG1 mRNA expression and up-regulates BCSG1 promoter activity through the intronic AP1 sites. The effect of TPA on BCSG1 transcription is also demonstrated under in vivo conditions in intact cells by using chromatin immunoprecipitation assays that show the TPA-induced binding of c-Jun to the chromatin region encompassing the intronic AP1 sites. Finally, to examine the direct effect of AP1 transactivation on BCSG1 expression, we established stable cell lines of T47D that express the dominant negative mutant of c-Jun, TAM67. RT-PCR and Western blot analyses demonstrated that levels of BCSG1 mRNA and protein in TAM67 transfectants were drastically reduced as compared with mock-transfected cells. Furthermore, inhibition of BCSG1 expression by blocking AP1 transactivation produced a similar repressive effect on cell growth as that by expressing BCSG1 antisense mRNA. We show that the anchorage-independent growth of T47D cells expressing either TAM67 or BCSG1 antisense mRNA is significantly inhibited. Taken together, we provide strong evidence that AP1 plays an overriding role in the transcription of the BCSG1 gene and that blockade of AP1 transactivation down-regulates BCSG1 expression and suppresses tumor phenotype. 

Retracted: No

PubPeer comments:
 There are several undeclared splicings in Western blot results, and some bands were not intact. ![file] ,
A New Taxonomy for Postactivation Potentiation in Sport
Authors: Alessandro Moura Zagatto
Irineu Loturco
Kenji Doma
David G Behm
Antonio Dello Iacono
Marco Beato
Francisco Cuenca-Fernández
Daniel Boullosa
Moritz Schumann
Journal: International journal of sports physiology and performance (2020)
Discipline: CLINICAL MEDICINE
Keywords: athletic performance; power; priming exercise; strength; warm-up.

Abstract:  Postactivation potentiation (PAP) mechanisms and responses have a long scientific history. However, to this day there is still controversy regarding the mechanisms underlying enhanced performance after a conditioning activity. More recently, the term postactivation performance enhancement (PAPE) has been proposed with differing associated mechanisms and protocols than with PAP. However, these 2 terms (PAP and PAPE) may not adequately describe all specific potentiation responses and mechanisms and can also be complementary, in some cases. Purpose: This commentary presents and discusses the similarities and differences between PAP and PAPE and, subsequently, elaborates on a new taxonomy for better describing performance potentiation in sport settings. Conclusion: The elaborated taxonomy proposes the formula "Post-[CONDITIONING ACTIVITY] [VERIFICATION TEST] potentiation in [POPULATION]." This taxonomy would avoid erroneous identification of isolated physiological attributes and provide individualization and better applicability of conditioning protocols in sport settings. 

Retracted: No

PubPeer comments:
 ![file] The marked results did not make sense. For patients with adenocarcinoma, the HR=0.7 and 95% CI from 0.39 to 1.26, in this situation, the p value must be **more than** 0.05 thus could not be 0.02. For patients with SCC, the HR=1.56 and 95% CI from 1.03 to 2.63, in this situation, the p value must be **less than** 0.05 thus could not be 0.23. , 
 Need to provide raw data to repeat stat analysis , 
 I am a statistical researcher and a reader of this article asked me about statistical concerns. After careful examination, I think the provided results really need further check. Here are my opinions. In cox model and the most commonly used Wald test for HR, we have ![file] And in N(0,1) of normal distribution, 95% CI correspond to 1.96 of Z value, ![file] (ref:https: onlinestatbook.com 2 estimation mean.html) Thus, we can get ![file] According to (1)(2)and (3), we could infer SE(beta) from 95% CI and calculate p value. ![file] For example, in above context of a and b, we could infer, a, if HR =0.66 and 95% CI is 0.47 to 0.94 the beta value is -0.408 and SE(beta) is 0.177, thus the p value is 0.0209.(accordant to context) b, if HR=0.58 and 95% CI is 0.37 to 0.91, the beta value is -0.544 , SE(beta)= 0.580, thus the p value should be 0.0178.(not accordant to context ) ,
Toxicity, toxicokinetics and biodistribution of dextran stabilized Iron oxide Nanoparticles for biomedical applications
Authors: A Sabareeswaran
P V Mohanan
S Syama
N S Remya
Journal: International Journal of Pharmaceutics (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Bio distribution; Biocompatibility; Dermal toxicity; Dextran stabilized iron oxide nanoparticle; Genotoxicity
Affiliations: Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Poojapura, Trivandrum 695 012, Kerala, India., Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Poojapura, Trivandrum 695 012, Kerala, India. Electronic address: .

Abstract:  Advancement in the field of nanoscience and technology has alarmingly raised the call for comprehending the potential health effects caused by deliberate or unintentional exposure to nanoparticles. Iron oxide magnetic nanoparticles have an increasing number of biomedical applications and hence a complete toxicological profile of the nanomaterial is therefore a mandatory requirement prior to its intended usage to ensure safety and to minimize potential health hazards upon its exposure. The present study elucidates the toxicity of in house synthesized Dextran stabilized iron oxide nanoparticles (DINP) in a regulatory perspective through various routes of exposure, its associated molecular, immune, genotoxic, carcinogenic effects and bio distribution profile. Synthesized ferrite nanomaterials were successfully coated with dextran (&lt;25nm) and were physicochemically characterized and subjected to in vitro and in vivo toxicity evaluations. The results suggest that surface coating of ferrite nanoparticles with dextran helps in improvising particle stability in biological environments. The nanoparticles do not seem to induce oxidative stress mediated toxicological effects, nor altered physiological process or behavior changes or visible pathological lesions. Furthermore no anticipated health hazards are likely to be associated with the use of DINP and could be concluded that the synthesized DINP is nontoxic/safe to be used for biomedical applications. 

Retracted: No

PubPeer comments:
 The Figure 8 in this paper has some unusual similarities with another paper from the same research group. Could the authors clarify? ![file] ![file] ,
Immunoglobulin gene rearrangement analysis in cerebrospinal fluid of patients with lymphoproliferative processes
Authors: Fred H Hochberg
Rebecca A Betensky
Jeffrey Sklar
Janina Longtine
Joachim M Baehring
Journal: Journal of the Neurological Sciences (2006)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: sensitivity; specificity; clonal immunoglobulin heavy chain gene rearrangement (IGHR) analysis; benign lymphoproliferative diseases; CSF samples
Affiliations: Pappas Center for Neuro-Oncology, Yawkey 9E, Massachusetts General Hospital, Boston, MA 02114, USA. 

Abstract:  Objective: To determine the sensitivity and specificity of clonal immunoglobulin heavy chain gene rearrangement (IGHR) analysis in the distinction of benign and malignant lymphoproliferative diseases. Methods: A retrospective analysis was conducted of patients in whom a malignant lymphoproliferative process was suspected. Cells of CSF samples were collected by centrifugation, resuspended in 100 microl of the supernatant and boiled. A 10 microl aliquot of this lysate served as template for semi-nested polymerase chain reaction using variable and joining region consensus primers. PCR products were analyzed by polyacrylamide gel electrophoresis. Cytopathological diagnosis and flow cytometry results were recorded. Sensitivity and specificity of IGHR analysis, cytopathology and flow cytometry were calculated. Results: Eleven patients (12 specimens) had involvement of leptomeninges at the time of lumbar puncture. Another 25 cases (27 specimens) had normal CSF findings or were diagnosed with benign lymphoproliferative conditions. Sensitivity of CSF cytopathology, flow cytometry and IGHR analysis were 0.27 [95% confidence interval 0.06, 0.61], 0.1 [0.003, 0.45] and 0.58 [0.28, 0.85]. Specificity was 1 [0.86, 1], 0.95 [0.77, 1.0] and 0.85 [0.66, 0.96]. Interpretation: IGHR analysis appears to be a useful addition to morphological and flow cytometry analysis of cerebrospinal fluid in the evaluation of CNS lymphoproliferative processes. 

Retracted: No

PubPeer comments:
 Concerns about Figure 1. * Splices are observed in most blots * Red boxes: Three lanes portraying patient 6 look like three lanes portraying patient 11. The other lanes are different. ![file] ,
Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation
Authors: Stephen C Strom
Giuseppa Augello
Caterina Di Sano
Giuseppe Montalto
James A McCubrey
Maria R Emma
Antonina Azzolina
Melchiorre Cervello
Daniele Balasus
Roberto Gramignoli
Antonella Cusimano
Journal: International Journal of Oncology (2017)
Discipline: CLINICAL MEDICINE
Keywords: Mediterranean diet; extra-virgin olive oil; oleocanthal; anti-inflammatory; cyclooxygenase
Affiliations: Institute of Biomedicine and Molecular Immunology 'Alberto Monroy', National Research Council (CNR), Palermo, Italy., Division of Pathology, Department of Laboratory Medicine, Cell Transplantation and Regenerative Medicine, Karolinska Institutet, Stockholm, Sweden., Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA.

Abstract:  The beneficial health properties of the Mediter-ranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW480) cell lines was used. Cells were treated with OC, and cell viability and apoptosis were evaluated. Compared with classical commercially available COX inhibitors (ibuprofen, indomethacin, nimesulide), OC was more effective in inducing cell growth inhibition in HCC and CRC cells. Moreover, OC inhibited colony formation and induced apoptosis, as confirmed by PARP cleavage, activation of caspases 3/7 and chromatin condensation. OC treatment in a dose dependent-manner induced expression of γH2AX, a marker of DNA damage, increased intracellular ROS production and caused mitochondrial depolarization. Moreover, the effects of OC were suppressed by the ROS scavenger N-acetyl-L-cysteine. Finally, OC was not toxic in primary normal human hepatocytes. In conclusion, OC treatment was found to exert a potent anticancer activity against HCC and CRC cells. Taken together, our findings provide preclinical support of the chemotherapeutic potential of EVOO against cancer. 

Retracted: No

PubPeer comments:
 Figure 5D may include an undisclosed splice. Could the authors review and comment? Brought to my attention by another reader who pointed out there appear to be other papers with concerns by one or more overlapping authors posted on PubPeer: https: pubpeer.com search?q=mccubrey https: pubpeer.com search?q=alberto+martelli https: pubpeer.com search?q=luca+neri https: pubpeer.com search?q=Lucio+Cocco https: pubpeer.com search?q=bruno+venerando *** Inverse image ![file] *** Original ![file] *** Full figure ![file] ,
RETRACTED: Obesity and mortality of COVID-19. Meta-analysis
Authors: Zefeng Xia
Shamsi El-Hasani
Wah Yang
Kamal Mahawar
Abdulzahra Hussain
Journal: Obesity Research & Clinical Practice (2020)
Discipline: CLINICAL MEDICINE
Keywords: Body mass index; COVID-19; Intensive care unit; Mortality; Obesity
Affiliations: Doncaster and Bassetlaw Teaching Hospitals, Doncaster, UK, Honorary Lecturer at Sheffield University, Sheffield, UK. Electronic address: ., Bariatric Unit, Department of General Surgery, Sunderland Royal Hospital, Sunderland, UK., Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei Province, China., The First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Guangzhou, Guangdong Province, China., Bariatric Unit, Princess Royal University Hospital, King's College Hospitals NHS Foundation Trust, London, UK.

Abstract:  Background: Obesity is a global disease with at least 2.8 million people dying each year as a result of being overweight or obese according to the world health organization figures. This paper aims to explore the links between obesity and mortality in COVID-19. Methods: Electronic search was made for the papers studying obesity as a risk factor for mortality following COVID-19 infection. Three authors independently selected the papers and agreed for final inclusion. The outcomes were the age, gender, body mass index, severe comorbidities, respiratory support and the critical illness related mortality in COVID-19. 572 publications were identified and 42 studies were selected including one unpublished study data. Only 14 studies were selected for quantitative analysis. Results: All the primary points but the gender are significantly associated with COVID-19 mortality. The age &gt;70, [odd ratio (OR): 0.17, CI; 95%, P-value: &lt;0.00001], gender [OR: 0.89; CI: 95%, P-value: 0.32], BMI &gt; 25 kg/m2 [OR: 3.68, CI: 95%, P-value: &lt;0.003], severe comorbidities [OR: 1.84, CI:95%, P-value: &lt;0.00001], advanced respiratory support [OR: 6.98, CI: 95%, P-value: &lt;0.00001], and critical illness [OR: 2.03, CI: 95%, P-value: &lt;0.00001]. Conclusions: Patients with obesity are at high risk of mortality from COVID-19 infection. 

Retracted: Yes

PubPeer comments:
 Figure 7A. Much more similar after vertical stretch than expected. https: imgur.com SndnWEt ,
Circ_001680 aggravates the malignant process of gastric carcinoma by targeting MAP2
Authors: W-D Chen
X-J Ding
Y Cai
S-Y Wang
X-S Wu
C Kan
Z-G Xia
Y Ma
H-D Zhao
J-J Cheng
L-Z Zhang
X-Y Wang
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: circ_001680; gastric carcinoma; clinicopathological parameters; metastasis; prognosis
Affiliations: Department of Emergency Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China. .

Abstract:  Objective: This study aims to explore the expression pattern and clinical significance of circ_001680 in gastric carcinoma (GC) process. Patients and methods: Circ_001680 levels in 40 pairs of GC and paracancerous ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between circ_001680 and GC clinicopathological parameters was analyzed. AGS and SGC-7901 cells were used for constructing circ_001680 knockdown models by shRNA transfection. Proliferative and metastatic abilities in GC cells with circ_001680 knockdown were examined by cell counting kit-8 (CCK-8) and transwell assay, respectively. Dual-Luciferase reporter assay was conducted to clarify the interaction between circ_001680 and MAP2. Their co-regulation on GC process was detected through rescue experiments. Results: Circ_001680 was highly expressed in GC tissues and cell lines. High level of circ_001680 predicted high incidences of lymphatic and distant metastasis, and poor prognosis in GC patients. Knockdown of circ_001680 suppressed proliferative and metastatic abilities in AGS and SGC-7901 cells. MAP2 was the target gene binding circ_001680, which was lowly expressed in GC. In addition, MAP2 was negatively correlated to circ_001680. Knockdown of MAP2 could abolish the suppressed proliferative and metastatic abilities in GC cells with circ_001680 knockdown. Conclusions: Circ_001680 is highly expressed in GC tissues and closely related to metastasis and prognosis in GC patients, which promotes the proliferative and metastatic abilities in GC cells by negatively interacting with MAP2. 

Retracted: No

PubPeer comments:
 Table 1. Column heads promise to convert numbers within each subgroup of patients into percentages, but do not deliver. ![file] , 
 This is a peculiar pair of Kaplan-Meier plots, with the crenellations along the tops of both curves so that they resemble combs, or walls constructed out of Lego. Similar plots, though, appear regularly within a genre of ERMPS papers. ![file] , 
 Fig 2C.  Migration and invasion in AGS and SGC-7901 cells with circ_001680 knockdown . Overlap marked. ![file] ,
MicroRNA-338 inhibits migration and proliferation by targeting hypoxia-induced factor 1α in nasopharyngeal carcinoma
Authors: Qicheng Zhang
Si Shi
Bo You
Xingyu Li
Ying Shan
Yiwen You
Journal: Oncology Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: Nasopharyngeal cancer; miR-338-3p; HIF-1α; cell proliferation; migration
Affiliations: Department of Ear, Nose and Throat, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China., Department of Pathology, Medical School of Nantong University, Nantong, Jiangsu 226001, P.R. China.

Abstract:  Nasopharyngeal cancer (NPC) is an endemic type of head and neck cancer with a high rate of cervical lymph node metastasis. An increasing number of studies have shown that microRNAs (miRNAs) play a key role in the development and progression of NPC. miR-338-3p has been demonstrated as an anti-oncogene in different solid tumors. The aim of the present study was to investigate the potential role of miR‑338-3p in the development and progression of NPC. Compared with normal samples, our data showed that miR-338-3p were downregulated in NPC tissues and cells. The luciferase assay demonstrated that HIF-1α was a direct target of miR-338-3p. We also found that miR-338-3p regulated the expression levels of HIF-1α, respectively. Overexpression of miR-338-3p in NPC cells significantly inhibited cell proliferation, and migration. Conversely, miR-338-3p knockdown in cells with lower endogenous expression levels significantly reduced antitumor behavior. Furthermore, enforced expression of miR-338-3p led to a decline in ERK phosphorylation as well as inhibited the hypoxia induced epithelial to mesenchymal transition. Cells pre-transfected with miR-338-3p can overcome hypoxia-mediated cisplatin resistance. Taken together, we found that miR-338-3p directly targeted HIF-1α, and we provide insight into NPC initiation and progression, possibly representing a novel therapeutic target. 

Retracted: No

PubPeer comments:
 Figure 4 appears to have an image overlap ![file] , 
 Corrigendum, [27 June 2022] .  Subsequently to the publication of the above article, an interested reader drew to the authorsu2019 attention that, for the cell migration assay data shown in Fig. 4B, the data panels representing the u2018miRu2011NC inhibitoru2019 and u2018hypoxiau2019 experiments appeared to contain overlapping sections, such that they may have been derived from the same original source. The authors have reu2011examined their original data, and realize that Fig. 4B was assembled incorrectly. A corrected version of Fig. 4, showing in Fig. 4B the data from one of the repeated cell migration assay experiments, is shown on the next page. The authors confirm that these data continue to support the main conclusions presented in their paper, and are grateful to the Editor of Oncology Reports for allowing them this opportunity to publish this Corrigendum. They also apologize to the readership for any inconvenience caused.  ,
LncRNA DLEU1 accelerates the malignant progression of clear cell renal cell carcinoma via regulating miRNA-194-5p
Authors: Y Zheng
Q-P Zhou
G-Z He
Z-Y Han
Y-W Zhang
S-Y Yu
J Yu
M-L Chen
Z-B Zhang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; DLEU1; miRNA-194-5p; ccRCC; metastasis
Affiliations: Department of Ultrasound, University of Chinese Academy of Sciences Shenzhen Hospital, Department of Interventional Ultrasound, Chinese PLA General Hospital, Shenzhen, China. .

Abstract:  Objective: The aim of this study was to illustrate the role of long non-coding RNA (lncRNA) DLEU1 in regulating the malignant progression of clear cell renal cell carcinoma (ccRCC) by targeting microRNA-194-5p (miRNA-194-5p). Patients and methods: DLEU1 expression level in ccRCC tissues and para-cancerous tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between DLEU1 expression and pathological indexes of ccRCC patients was assessed. After the silence of DLUE1, the proliferative and migratory abilities of ACHN and 786-O cells were evaluated. Furthermore, Dual-Luciferase reporter gene assay and rescue experiments were conducted to identify the role of DLEU1/miRNA-194-5p in regulating the ccRCC progression in vitro. Results: DLEU1 expression was markedly up-regulated in ccRCC tissues when compared with para-cancerous tissues. The rates of lymphatic metastasis and distant metastasis in ccRCC patients with a high level of DLEU1 were significantly higher, whereas the prognosis was significantly worse. Transfection of si-DLEU1 remarkably attenuated proliferative and migratory abilities of ACHN and 786-O cells. MiRNA-194-5p was identified as the target gene of DLEU1. In addition, the knockdown of miRNA-194-5p could reverse the regulatory effect of DLEU1 on the proliferative and metastatic abilities of ccRCC. Conclusions: DLEU1 is closely related to lymphatic metastasis, distant metastasis, and poor prognosis of ccRCC. It aggravates the progression of ccRCC by targeting miRNA-194-5p. 

Retracted: Yes

PubPeer comments:
 November 2020 retraction notice without details. It says that the article  has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. One finding for Figure 2D: * Cyan boxes: two panels appear to show the same region, but at a 90 degree angle, which suggests that these are not just two overlapping photos. ![file] , 
 Another finding for Figure 2C. Figure 2C: * Purple boxes: possible overlap with a panel in Figure 2C of Hao Wu et al., JBUON (2020), PMID: 32521900 - https: pubpeer.com publications 76307B2F002B5EBBA5EC4DE7A873B5 ![file] , 
 Another finding in Figure 2D: Light green boxes highlight an overlapping area, again with a 90 degrees rotation, with Figure 3 in Hao Wu et al., JBUON (2020), PMID: 32521900 - https: pubpeer.com publications 76307B2F002B5EBBA5EC4DE7A873B5 ![file] ,