PReD-Bench/PRed-Bench huggingface dataset:
Intragenic deletion in the Desmoglein 4 gene underlies the skin phenotype in the Iffa Credo “hairless” rat
Authors: Hisham Bazzi
Andrey A Panteleyev
Angela M Christiano
Ana Kljuic
Journal: Differentiation (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Iffa Credo; hairless rat; autosomal recessive; hypotrichotic; pharmacological studies
Affiliations: Department of Genetics & Development, Columbia University, New York, NY 10032, USA.

Abstract:  The Iffa Credo (IC) "hairless" rat is an autosomal recessive hypotrichotic animal model actively used in pharmacological and dermatological studies. Although the molecular basis of the IC rat phenotype was never defined, the designation "hr/hr" (hairless) has been used for this rat mutation. Despite the observation that IC rats share many phenotypic similarities with Charles River (CR) 'hairless rats', crossbreeding between CR and IC rats indicated that these mutations are not allelic, and moreover, genetic analysis of both CR and IC hairless mutant rats showed no mutations in the hr gene. Here, we present a detailed analysis of the skin phenotype in the IC rat. While the initial stages of hair follicle (HF) morphogenesis reveal no significant abnormalities, the subsequent processes of inner root sheath and hair shaft formation are severely disturbed due to impaired proliferation in the hair matrix and abnormal differentiation in the precortex zone. This results in significant reduction of hair bulb volume, and the formation of dysmorphic "blebbed" hair shafts lacking medullar structure and resembling "lanceolate" hairs. Based on the presence of lance-head hairs typical of rodent lanceolate mutants, we performed molecular analysis of the desmoglein 4 gene and found a large intragenic deletion encompassing nine exons of the gene. This finding, together with specific morphological features of skin and hairs, confirms that the IC rat is allelic with the lanceolate hair (lah) mutations in mice and rats. Our results elucidate the genetic and morphological basis of the IC rat mutation, thus providing a new model to study molecular mechanisms of hair growth control. 

Retracted: No

PubPeer comments:
 Possible band duplication published in different papers ![file] ,
Three novel missense mutations in the filamin B gene are associated with isolated congenital talipes equinovarus
Authors: Huimin Li
Xiaoqing Zhang
Qihua Fu
Zhigang Wang
Xingchen Ye
Haiqing Cai
Zhaojing Zheng
Haiou Yang
Journal: Human Genetics (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Congenital talipes equinovarus; CTEV; Genetic factors; PITX1; TBX4
Affiliations: Department of Laboratory Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China., Department of Pediatric Orthopedics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China., Department of Pediatric Orthopedics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China. ., Department of Laboratory Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, People's Republic of China. .

Abstract:  Congenital talipes equinovarus (CTEV) is one of the most common musculoskeletal disorders. Genetic factors have been suggested to be an important contributor to its pathogenesis. Some genes, including PITX1, TBX4, and RBM10, have been associated with CTEV. We aimed to determine the disease-causing mutations in Chinese patients with isolated CTEV. Genomic DNA was extracted from peripheral blood samples of a three-generation pedigree and 53 sporadic patients with CTEV. Whole-exome sequencing and Sanger sequencing were used to identify and validate disease-causing mutations, respectively. A putative pathogenic mutation c.4717G&gt;T (p.D1573Y) in the filamin B (FLNB) gene, which co-segregated with CETV, was identified in the pedigree. Two additional novel missense mutations in the same gene [c.1897A&gt;G (p.M633V) and c.2195A&gt;G (p.Y732C)] were identified from the 53 sporadic patients. Plasmids expressing wild-type or mutant constructs were transfected into HEK293T cells to determine whether these amino acid substitutions affect protein activity. All three (M633V, Y732C, and D1573Y) affected FLNB protein expression and led to cytoplasmic focal accumulation. Our results provide evidence for the involvement of FLNB in the pathogenesis of isolated CTEV and have expanded the clinical spectrum of FLNB mutations. 

Retracted: No

PubPeer comments:
 The paper contains a high degree of overlap with other works published by the same author around the same time. See example below. ![file] ,
MKP-1 regulates cytokine mRNA stability through selectively modulation subcellular translocation of AUF1
Authors: Viswanathan Palanisamy
Keith L Kirkwood
Courtney Haycraft
Hong Yu
Yuhao Sun
Journal: Cytokine (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MAPK phosphatase-1; DUSP-1; cytokine expression; post-transcriptional level; activated MAPK responses
Affiliations: Department of Craniofacial Biology and the Center for Oral Health Research, Medical University of South Carolina, SC 29425, United States.

Abstract:  MAPK phosphatase-1 (MKP-1)/dual specificity protein phosphatase-1 (DUSP-1) is a negative regulator of the host inflammatory response to infection. However, the mechanisms underlying the regulation of cytokine expression by MKP-1, especially at the post-transcriptional level, have not been fully delineated. In the current study, MKP-1 specifically dephosphorylated activated MAPK responses and attenuated LPS-induced IL-6, IL-10, and TNF-α expression. In addition, MKP-1 was important in destabilizing cytokine mRNAs. In LPS-stimulated rat macrophages with overexpressed MKP-1, half-lives of IL-6, IL-10 and TNF-α mRNAs were significantly reduced compared to controls. Conversely, half-lives of IL-6, IL-10, and TNF-α mRNAs were significantly increased in bone marrow macrophages derived from MKP-1 knock out (KO) mice compared with macrophages derived from MKP-1 wild type (WT) mice. Furthermore, MKP-1 promoted translocation of RNA-binding protein (RNA-BP) ARE/poly-(U) binding degradation factor 1 (AUF1) from the nucleus to the cytoplasm in response to LPS stimulation as evidenced by Western blot and immunofluorescent staining. Knockdown AUF1 mRNA expression by AUF1 siRNA in MKP-1 WT bone marrow macrophages significantly delayed degradation of IL-6, IL-10 and TNF- α mRNAs compared with controls. Finally, AUF1 was immunoprecipitated with the RNA complex in cellular lysates derived from bone marrow macrophages of MKP-1 KO vs. WT mice, which had increased AUF1-bound target mRNAs, including IL-6, IL-10, and TNF-α in WT macrophages compared with MKP-1 KO macrophages. Thus, this work provides new mechanistic insight of MKP-1 signaling and regulation of cytokine mRNA stability through RNA binding proteins in response to inflammatory stimuli. 

Retracted: No

PubPeer comments:
 Figure 1. * Red boxes: Two MKP-1 panels appear to look more similar than expected. Contrast enhanced to bring out details. ![file] Reported to the journal in October 2015. ,
On making the right choice: the deliberation-without-attention effect
Authors: Maarten W Bos
Loran F Nordgren
Rick B van Baaren
Ap Dijksterhuis
Journal: Science (2006)
Discipline: Multidisciplinary
Keywords: conscious deliberation; unconscious thought; simple choices; complex matters; deliberation-without-attention hypothesis
Affiliations: Department of Psychology, University of Amsterdam, Roetersstraat 15, 1018 WB, Amsterdam, the Netherlands. 

Abstract:  Contrary to conventional wisdom, it is not always advantageous to engage in thorough conscious deliberation before choosing. On the basis of recent insights into the characteristics of conscious and unconscious thought, we tested the hypothesis that simple choices (such as between different towels or different sets of oven mitts) indeed produce better results after conscious thought, but that choices in complex matters (such as between different houses or different cars) should be left to unconscious thought. Named the "deliberation-without-attention" hypothesis, it was confirmed in four studies on consumer choice, both in the laboratory as well as among actual shoppers, that purchases of complex products were viewed more favorably when decisions had been made in the absence of attentive deliberation. 

Retracted: No

PubPeer comments:
 These results have been proven to be difficult to replicate. There is conclusive evidence that the main author of this article, Ap Dijksterhuis, used questionable practices in general. https: replicationindex.com 2021 01 19 personalized-p-values To interpret results published during this time with caution, it is useful to use a more stringent significance criterion of p .005 to guard against false positive results. This article reported four studies with small samples and all p-values are greater than .005; .03, .02, .04, .02. The fact that all four studies are significant does not show that there is a real effect. It merely shows that results were selected for significance. Hence, this article should no longer be cited as empirical evidence for the claims made in this article. ,
JMJD3 enhances invasiveness and migratory capacity of non-small cell lung cancer cell via activating EMT signaling pathway
Authors: G-X Zhang
B Wang
P-Y Hua
Y Zhang
C-Y Jin
J-D Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: JMJD3; non-small cell lung cancer; clinical features; prognosis; qRT-PCR
Affiliations: Department of Thoracic Surgery, The Second Hospital of Jilin University, Changchun, China. .

Abstract:  Objective: This study aimed to explore the expression of JMJD3 in non-small cell lung cancer (NSCLC) and to further study its association with clinical features and prognosis of patients. Patients and methods: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the level of JMJD3 in 46 pairs of NSCLC tissues and para-cancerous specimens. The relationship between JMJD3 level and clinical features of NSCLC and patients' prognosis was analyzed. And JMJD3 expression in NSCLC cells was further verified by qRT-PCR. In addition, JMJD3 knockdown model was constructed using siRNA in cell lines including A549 and SPC-A1, and the effect of JMJD3 on the biological function of NSCLC cells was analyzed by cell counting kit-8 (CCK-8) and transwell migration and invasive-ness assays. Lastly, Western blot was performed to explore the potential mechanism. Results: In this investigation, qRT-PCR results indicated that JMJD3 expression in above-mentioned tumor tissues was conspicuously higher than that in normal tissues. In addition, compared with patients with low level of JMJD3, patients with high level of JMJD3 had a higher incidence of lymphatic metastasis and distant metastasis and a lower overall survival rate. Meanwhile, the proliferation, invasiveness and migratory capacity of cells in the sh-JMJD3 group was conspicuously decreased when compared with the cells in negative control group. Western Blot results indicated that the levels of key proteins in EMT signaling pathway such as E-cadherin, N-cadherin, Vimentin, TGF-β, and MMP-9 were notably decreased in sh-JMJD3 group. Besides, the addition of TGF-β cytokines synergistically promoted the malignant progression of NSCLC induced by JMJD3. Conclusions: JMJD3 expression was found conspicuously increased in NSCLC, which might be close relevant to NSCLC lymphatic or distant metastasis as well as patients' poor prognosis. Therefore, we speculated that JMJD3 could promote invasiveness and migratory capacity of non-small cell lung cancer cells by activating EMT process. 

Retracted: No

PubPeer comments:
 Figure 2D.  Proliferation, invasion, and migration of non-small cell lung cancer cells were inhibited after silencing JMJD3. ... D, Transwell migration and invasion assay detected the invasion and migration of non-small cell lung cancer cells after interference with JMJD3 in A549 ... cell lines . Overlaps marked. ![file] ,
Tracking Changes in SARS-CoV-2 Spike: Evidence that D614G Increases Infectivity of the COVID-19 Virus
Authors: Charlene McDanal
Nick Hengartner
Luke R Green
Matthew D Parker
Dennis Wang
Hyejin Yoon
Rebecca L Brown
Thushan I de Silva
Danielle C Groves
Adrienne Angyal
Celia C LaBranche
Katie J Johnson
Kathryn M Hastie
Benjamin B Lindsey
David G Partridge
Brian Foley
Matthew D Wyles
Haili Tang
Sandrasegaram Gnanakaran
Sean P Whelan
Erica O Saphire
Alex Moon-Walker
Rachel M Tucker
Nikki Smith
James Theiler
Mohammad Raza
Alexander J Keeley
Timothy M Freeman
Paul J Parsons
Will M Fischer
Elena E Giorgi
Sarah Rowland-Jones
Tanmoy Bhattacharya
Cariad M Evans
Werner Abfalterer
Sheffield COVID-19 Genomics Group
Bette Korber
David C Montefiori
Laura Carrilero
Lautaro G Perez
Journal: Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: COVID-19; PCR cycle threshold; SARS-CoV-2; Spike; antibody

Abstract:  A SARS-CoV-2 variant carrying the Spike protein amino acid change D614G has become the most prevalent form in the global pandemic. Dynamic tracking of variant frequencies revealed a recurrent pattern of G614 increase at multiple geographic levels: national, regional, and municipal. The shift occurred even in local epidemics where the original D614 form was well established prior to introduction of the G614 variant. The consistency of this pattern was highly statistically significant, suggesting that the G614 variant may have a fitness advantage. We found that the G614 variant grows to a higher titer as pseudotyped virions. In infected individuals, G614 is associated with lower RT-PCR cycle thresholds, suggestive of higher upper respiratory tract viral loads, but not with increased disease severity. These findings illuminate changes important for a mechanistic understanding of the virus and support continuing surveillance of Spike mutations to aid with development of immunological interventions. 

Retracted: No

PubPeer comments:
 https: twitter.com MoNscience status 1279839791731875842 , 
 Spike mutation D614G alters SARS-CoV-2 fitness https: www.nature.com articles s41586-020-2895-3 ,
Low-level PDT treatment modulated photoaging mediated by UVA irradiation through regulating Bach2
Authors: Mei Wang
Xia Lei
Jinyi Chen
Yan Wu
Jiefu Luo
Li Chang
Zhong Li
Xing Yang
Journal: Photodiagnosis and photodynamic therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: Bach2; Fibroblasts; PDT; Photoaging; UVA.
Affiliations: Key Laboratory of Biorheological Science and Technology, Ministry of Education, Chongqing University, Chongqing 400044, China; Department of Dermatology, Daping Hospital, The Army Medical University. Chongqing, 400042, China. Electronic address: ., Key Laboratory of Biorheological Science and Technology, Ministry of Education, Chongqing University, Chongqing 400044, China. Electronic address: ., Department of Dermatology, Daping Hospital, The Army Medical University. Chongqing, 400042, China. Electronic address: .

Abstract:  Objective: To investigate low-level ALA-PDT (Aminolevulinic acid photodynamic therapy) effects on photorejuvenation in vitro and in vivo, exploring the basic mechanism of Bach2 involved in PDT treatment in photoaging. Method: Photoaging model was established by UVA chronic irradiation in human fibroblasts and mice skins. Cell viability was determined by MTS assay and cell senescence was detected by SA-β-gal activity. PDT treatment and Bach2 knockdown with adenovirus in fibroblasts were confirmed by Western blot. Results: UVA chronic irradiation induced photoaging in vitro and in vivo. Treatment of low-level PDT reduced photoaging by decreasing SA-β-gal activity and cell senescence-related proteins levels of p16 and p21 in fibroblasts. Moreover, low-level PDT treatment accompany with Bach2 accumulation increased in fibroblasts and in mice skin tissues. Bach2 knockdown with adenovirus induced cell senescence and Bach2 depletion with PDT treatment some extent decreased SA-β-gal activity, but was with no significant change of Bach2 itself and p16 protein levels in fibroblasts. Conclusion: Low-level PDT treatment decreased skin photoaging which might be through up-regulating Bach2. 

Retracted: No

PubPeer comments:
 ![file] In figure 5A, the pictures of different groups (marked in red) were obviously duplicated. , 
 Thank you for your find this issue, I am apologize for my mistakes, i will apply for the PDPDT journal to correct it. Thank you again. ,
Novel role of famotidine in downregulation of matrix metalloproteinase-9 during protection of ethanol-induced acute gastric ulcer
Authors: Laishram Pradeepkumar Singh
Krishnendu Ganguly
Snehasikta Swarnakar
Amartya Mishra
Parag Kundu
Journal: Free Radical Biology and Medicine (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Gastric ulcer; Matrix metalloproteinases (MMPs); ProMMP-9; Ethanol-induced; H(2)-receptor antagonists
Affiliations: Department of Physiology, Indian Institute of Chemical Biology, 4, Raja S.C. Mullick Road, Jadavpur, Kolkata 700032, India.

Abstract:  Gastric ulcer is a multifaceted process including acid secretion, reactive oxygen species generation, prostaglandin inhibition, and extracellular matrix (ECM) degradation. Matrix metalloproteinases (MMPs) have the ability to cleave and remodel the ECM. We investigated the activity and expression of MMP-9 and -2 in ethanol-induced acute gastric ulceration in rats. We found that severity of gastric ulcer was strongly correlated with increasing doses of ethanol and increased secretion of proMMP-9. ProMMP-9 was upregulated approximately 25-fold at maximum ulcer index. Increased secretion of proMMP-9 was associated with increased expression of tumor necrosis factor-alpha and interleukin-6. We examined the effect of H(2)-receptor antagonists and antioxidants on proMMP-9 secretion and synthesis during prevention of ethanol-induced gastric ulcer. Our data reveal that famotidine dose dependently blocked increased secretion and synthesis of proMMP-9 during gastroprotection and arrested infiltration of inflammatory cells as well as oxidative stress in rat gastric tissues. Similar to H(2)-receptor antagonists, N-acetylcysteine and dimethyl sulfoxide, well-known antioxidants, inhibited proMMP-9 upregulation to the control level. In conclusion, ethanol-induced gastric ulceration is associated with increased expression of proMMP-9 that can be attenuated by H(2)-receptor antagonists and antioxidants. These findings furnish a novel MMP-9-mediated pathway and its inhibition via proinflammatory cytokines by famotidine in ethanol-induced gastric ulceration. 

Retracted: No

PubPeer comments:
 Unexpected similarity between some bands in Fig 2A ![file] , 
 Unusual repeated artefacts in Fig 2C (red arrows) ![file] Zoom ![file] ,
RETRACTED ARTICLE: Complete mitochondrial genome of Paracobitis variegates and its phylogenetic analysis
Authors: Xing You Liu
Jian He Hu
Guang Hui Wei
Chang Zhong Liu
Journal: Mitochondrial DNA Part A (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Genome; mitochondrion; paracobitis variegates; phylogenetic analysis.
Affiliations: a College of Animal Science, Henan Institute of Science and Technology , Xinxiang , Henan Province , China.

Abstract:  In this study, the complete mitochondrial genome sequence of the Paracobitis variegates was first reported. The total length of the mitogenome is 16,571 bp long with the A + T content of 55.6%. It contains the typical structure, including 13 protein-coding genes, 22 transfer RNA genes, two ribosomal RNA genes, and one D-loop region. The protein-coding genes start with the typical ATG codon, while COI gene uses GTG as the initiation codon. Most tRNA genes could form typical secondary structures except tRNA(ser), which had an absence of the DHU arm. There are 43 helices structures in 12S rRNA, and six domains, 53 helices structures in 16S rRNA. According to the phylogenetic analysis, Paracobitis variegates has a closer relationship with Barbatula toni. 

Retracted: Yes

PubPeer comments:
 Retraction notice:  We, the Editor, authors and Publisher have retracted the following article: Liu, C.Z., Wei, G.H., Hu, J.H. Liu, X.Y. Complete mitochondrial genome of Paracobitis variegates [sic] and its phylogenetic analysis. Mitochondrial DNA Part A 27:4 (2016) 2421-2422. 10.3109 19401736.2015.1030624. The above article has been retracted as, subsequent to publication, duplication has been found in the article content and data with the following earlier published article: Shi, Y., Xing, L., Chen, T., Yang, M. You, P. u2018Sequencing and analysis of the complete mitochondrial genome of Paracobitis variegatusu2019. Journal of the Shaanxi Normal University 42:4 (2014) 50-56. The authors omitted to acknowledge the original publication of the mitogenome sequence in the Journal of the Shaanxi Normal University article, and presented this research as their own. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. https: www.tandfonline.com doi full 10.1080 24701394.2020.1758393 , 
 Backgrounds in a technical report at https: www.researchgate.net publication 337063445 ,
High‐mobility group box‐1 contributes tumor angiogenesis under interleukin‐8 mediation during gastric cancer progression
Authors: Jong-Baeck Lim
Hye Won Chung
Journal: Cancer Science (2017)
Discipline: CLINICAL MEDICINE
Keywords: Angiogenesis; cytokine; gastric cancer; high-mobility group box-1; interleukin-8.
Affiliations: Department of Laboratory Medicine, Seoul, Korea., Severance Institute for Vascular and Metabolic Research, Yonsei University College of Medicine, Seoul, Korea.

Abstract:  Many soluble factors are involved in tumor angiogenesis. Thus, it is valuable to identify novel soluble factors for effective control of tumor angiogenesis in gastric cancer (GC). We investigated the role of extracellular high-mobility group box-1 (HMGB1) and its associated soluble factors in the tumor angiogenesis of GC. Clinically, we measured serum levels of HMGB1 and GC-associated cytokines/chemokines using GC serum samples (n = 120), and calculated microvessel density (MVD) by CD34 immunostaining using human GC tissues (n = 27). Then we analyzed the correlation of serum HMGB1 levels with MVD or that with cytokine/chemokine levels by linear regression. As in vitro angiogenesis assay for HMGB1, HUVEC migration and capillary tube formation assay were carried out using different histological types of human GC cells (N87 and KATOIII). CD34-positive microvessels were detected from early GC, but MVD increased according to GC stages, and were closely correlated with serum HMGB1 levels (R = 0.608, P = 0.01). The HUVECs cultured in conditioned media derived from rhHMGB1-treated or HMGB1-TF GC cells showed remarkably enhanced migration and tube formation activities. These effects were abrogated by anti-HMGB1 antibody or HMGB1 siRNA in both N87 and KATOIII cells (all P &lt; 0.05). Among tested cytokines/chemokines, interleukin-8 (IL-8) was the most remarkable cytokine correlated with serum HMGB1 (P &lt; 0.001), and enhanced HUVEC migration and tube formation activities by rhHMGB1 or HMGB1-TF were significantly reversed by IL-8 inhibition. These results indicate overexpressed HMGB1 contributes to tumor angiogenesis through IL-8 mediation, and combined targeting of HMGB1 and IL-8 can control tumor angiogenesis in GC. 

Retracted: No

PubPeer comments:
 Figures 1 and 2 appear to have a repeated image, after rotation. Can the authors comment on whether this is deliberate? *** ![file] , 
 Figures four and six also seem to have images which overlap, with rotation and adjusted dimensions. *** ![file] ,
APC-Cdh1 Regulates Neuronal Apoptosis Through Modulating Glycolysis and Pentose-Phosphate Pathway After Oxygen-Glucose Deprivation and Reperfusion
Authors: Wenlong Yao
Chuanhan Zhang
Zuofan Li
Bo Zhang
Li Wan
Yue Zhang
Journal: Cellular and Molecular Neurobiology (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Aerobic glycolysis; Cdh1; Neuron; Oxygen-glucose deprivation; Pentose-phosphate pathway.
Affiliations: Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, China., Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, China. .

Abstract:  Anaphase-promoting complex (APC) with its coactivator Cdh1 is required to maintain the postmitotic state of neurons via degradation of Cyclin B1, which aims to prevent aberrant cell cycle entry that causes neuronal apoptosis. Interestingly, evidence is accumulating that apart from the cell cycle, APC-Cdh1 also involves in neuronal metabolism via modulating the glycolysis promoting enzyme, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3). Here, we showed that under oxygen-glucose deprivation and reperfusion (OGD/R), APC-Cdh1 was decreased in primary cortical neurons. Likewise, the neurons exhibited enhanced glycolysis when oxygen supply was reestablished during reperfusion, which was termed as the "neuronal Warburg effect." In particular, the reperfused neurons showed elevated PFKFB3 expression in addition to a reduction in glucose 6-phosphate dehydrogenase (G6PD). Such changes directed neuronal glucose metabolism from pentose-phosphate pathway (PPP) to aerobic glycolysis compared to the normal neurons, resulting in increased ROS production and apoptosis during reperfusion. Pretreatment of neurons with Cdh1 expressing lentivirus before OGD could reverse this metabolic shift and attenuated ROS-induced apoptosis. However, the metabolism regulation and neuroprotection by Cdh1 under OGD/R condition could be blocked when co-transfecting neurons with Ken box-mut-PFKFB3 (which is APC-Cdh1 insensitive). Based on these data, we suggest that the Warburg effect may contribute to apoptotic mechanisms in neurons under OGD/R insult, and targeting Cdh1 may be a potential therapeutic strategy as both glucose metabolic regulator and apoptosis suppressor of neurons in brain injuries. 

Retracted: No

PubPeer comments:
 similar pictures in figure 2c and 3a ![file] , 
 more similar than expected in figure 4a and 5d ![file] ,
Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death
Authors: R D Schreiber
G Nuñez
D Hockenbery
S J Korsmeyer
C Milliman
Journal: Nature (1990)
Discipline: Multidisciplinary
Keywords: t(14; 18) chromosomal translocation; bcl-2 gene; immunoglobulin heavy chain locus; deregulated
Affiliations: Department of Medicine, Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110.

Abstract:  The t(14; 18) chromosomal translocation of human follicular B-cell lymphoma juxtaposes the bcl-2 gene with the immunoglobulin heavy chain locus. The bcl-2 immunoglobulin fusion gene is markedly deregulated resulting in inappropriately elevated levels of bcl-2 RNA and protein. Transgenic mice bearing a bcl-2 immunoglobulin minigene demonstrate a polyclonal expansion of resting yet responsive IgM-IgD B cells which display prolonged cell survival but no increase in cell cycling. Moreover, deregulated bcl-2 extends the survival of certain haematopoietic cell lines following growth-factor deprivation. By using immunolocalization studies we now demonstrate that Bcl-2 is an integral inner mitochondrial membrane protein of relative molecular mass 25,000 (25k). Overexpression of Bcl-2 blocks the apoptotic death of a pro-B-lymphocyte cell line. Thus, Bcl-2 is unique among proto-oncogenes, being localized to mitochondria and interfering with programmed cell death independent of promoting cell division. 

Retracted: No

PubPeer comments:
 Only problem is Bcl-2 is not an inner mitochondrial membrane protein. See PMID 1453000 ,
Induction of hsp70, hsp60, hsp83 and hsp26 and oxidative stress markers in benzene, toluene and xylene exposed Drosophila melanogaster: role of ROS generation
Authors: M M Krishna Reddy
D K Saxena
N Mathur
Mahendra Pratap Singh
D Kar Chowdhuri
Journal: Toxicology and Applied Pharmacology (2009)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: benzene; toluene; xylene; Drosophila melanogaster; heat shock proteins
Affiliations: Embryotoxicology Section, Indian Institute of Toxicology Research, P.O. Box No. 80, Mahatma Gandhi Marg, Lucknow- 226 001, Uttar Pradesh, India.

Abstract:  Exposure to benzene, toluene and xylene in the human population may pose a health risk. We tested a working hypothesis that these test chemicals cause cellular toxicity to a non-target organism, Drosophila melanogaster. Third instar larvae of D. melanogaster transgenic for hsp70, hsp83 and hsp26 and Oregon R(+) strain were exposed to 1.0-100.0 mM benzene, toluene and xylene for 2-48 h to examine the heat shock proteins (hsps), ROS generation, anti-oxidant stress markers and developmental end points. The test chemicals elicited a concentration- and time-dependent significant (p&lt;0.01) induction of the hsps in the exposed organism in the order of hsp70&gt;hsp83&gt;or=hsp26 as evident by beta-galactosidase activity after 24 h. RT-PCR amplification studies in Oregon R(+) larvae revealed a similar induction pattern of these genes along with hsp60 in the order of hsp70&gt;hsp60&gt;hsp26&gt;or=hsp83. Under similar experimental conditions, a significant induction of ROS generation and oxidative stress markers viz. superoxide dismutase, catalase, glutathione S-transferase, thioredoxin reductase, glutathione, malondialdehyde and protein carbonyl content was observed. Sub-organismal response was propagated towards organismal response i.e., a delay in the emergence of flies and their reproductive performance. While hsp70 was predominantly induced in the organism till 24 h of treatment with the test chemicals, a significant or insignificant regression of Hsp70 after 48 h was concurrent with a significant induction (p&lt;0.01) of hsp60&gt;hsp83&gt;or=hsp26 in comparison to the former. A significant positive correlation was observed between ROS generation and these hsps in the exposed organism till 24 h and a negative correlation between ROS generation and hsp70 in them after 48 h indicating a modulatory role of ROS in the induction of hsps. The study suggests that among the tested hsps, hsp70 may be used as an early bioindicator of cellular toxicity against benzene, toluene and xylene and D. melanogaster as an alternative animal model for screening the risk posed by environmental chemicals. 

Retracted: No

PubPeer comments:
 ![file] , 
 #1 Actually, if you look even more closely, the first 6 actin bands (starting from the right, and heading left) repeat themselves. ,
Ficus carica extract impregnated amphiphilic polymer scaffold for diabetic wound tissue regenerations
Authors: Shujin Wang
Xufeng Liu
Yu Niu
Yi Zhang
Jia Feng
Hong Zuo
Journal: Artificial Cells Nanomedicine and Biotechnology (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Diabetic wounds; Ficus carica; extracellular matrix; hypoxia; polymeric scaffold.
Affiliations: Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China, Department of Endocrinology, Ninth Hospital of Xi'an, Xi'an, China

Abstract:  Diabetes associated injury healing and other tissue irregularities are viewed as a significant concern. The purpose of the study is to design the wound regeneration activity of Ficus carica extract (FFE) loaded amphiphilic polymeric scaffold of poly(xylitol-g-adipate-co-glutamide) (PXAG)-polyhydroxybutyrate (PHB) for potential diabetic affected wound regeneration. The PXAG copolymer was prepared by the condensation method, and the polymeric scaffolds of PXAG-PHB, PXAG-PHB/FFE were developed through the ultra-sonication process and magnetic stirrer processes. The chemical structure, crystalline nature, thermal stability, size, surface charge and surface morphology of PXAG-PHB and PXAG-PHB/FFE polymeric scaffolds were investigated. The PXAG-PHB/FFE exhibits 99.0% free radical scavenging activity which was determined by the DPPH method. The inhibition zones by the PXAG-PHB/FFE indicate it had a higher antibacterial activity with the Escherichia coli (gram-negative) and Staphylococcus aureus (gram-positive) pathogens. The PXAG, PXAG-PHB and PXAG-PHB/FFE polymeric scaffolds exhibited good viability against diabetic induced wound cells (WS1) in 100 μg/mL concentrations up to 72 h incubation. Since the synthesized PXAG-PHB/FFE polymeric scaffolds possess excellent thermal stability, bioactivity, biocompatibility and antioxidant activity along with potent antimicrobial activity, they play a potential role in diabetic wound tissue regenerations. 

Retracted: No

PubPeer comments:
 The image in Figure 4d does not correspond with the image in Figure 4e. ![file] ,
YM155 decreases radiation-induced invasion and reverses epithelial–mesenchymal transition by targeting STAT3 in glioblastoma
Authors: Jianxiong Ji
Anjing Chen
Bin Huang
Mingzhi Han
Yangyang Xu
Jian Wang
Xin Zhang
Yuzhen Wei
Xuehai Wang
Chen Qiu
Qing Zhang
Ran Xu
Wenjie Li
Xingang Li
Journal: Journal of Translational Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: Epithelial–mesenchymal transition; Glioblastoma; Radiation; STAT3; YM155.
Affiliations: Department of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, Jinan, 250012, People's Republic of China., Department of Otolaryngology, Weihai Municipal Hospital, Weihai, 264200, Shandong, People's Republic of China., Department of Neurosurgery, Jining No. 1, People's Hospital, Jining, 272011, China., Department of Biomedicine, University of Bergen, 5009, Bergen, Norway., Department of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, 250012, People's Republic of China. .

Abstract:  Background: Radiotherapy constitutes a standard arm of therapy in the multimodal treatment of patients with glioblastoma (GBM). Ironically, studies have recently revealed that radiation can augment malignant progression, by promoting migration and invasion, which make the disease especially difficult to cure. Here, we investigated the anticancer effects of YM155, a purported radiosensitizer, in GBM cell lines. Methods: GBM cell lines U251 and U87 were treated with YM155 to assess cytotoxicity and activity of the molecule in vitro. Nude mice were implanted with cells to generate orthotopic xenografts for in vivo studies. Response of cells to treatment was examined using cell viability, immunofluorescence, wound healing, and the Transwell invasion assay. Molecules potentially mediating response were examined through western blot analysis, phospho-kinase arrays, and qPCR. Cells were transfected with siRNA knockdown and gene expression constructs to identify molecular mediators of response. Results: YM155 reduced viability of U251 and U87 cells and enhanced radiosensitivity through inhibition of homologous recombination. Besides, YM155 decreased invasion caused by radiation and led to expression changes in molecular markers associated with EMT. STAT3 was one of 10 molecules identified on a phosphokinase array exhibiting significant change in phosphorylation under YM155 treatment. Transfection with STAT3 siRNAs or expression constructs demonstrated that EMT changes were achieved by inhibiting the phosphorylation of STAT3 and were survivin-independent. Finally, combining YM155 and radiation in orthotopic xenografts reduced growth and prolonged overall survival of animals. Conclusions: YM155 decreased radiation-induced invasion in GBM cell lines in vitro and in vivo through inhibition of STAT3. 

Retracted: No

PubPeer comments:
 In Figure 5f,h, a micrograph has been duplicated and presented as something else. ![file] ,
Analysis of Meiotic Segregation Patterns and Interchromosomal Effects in Sperm from 13 Robertsonian Translocations
Authors: Z Liu
B Wang
X Liu
J Song
D Tang
B Nie
W Wang
R Li
Journal: Balkan Journal of Medical Genetics (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Evolution; Interchromosomal effects; Meiotic segregation; Robertsonian (ROB) translocation homozygosity; Sperm fluorescence in situ hybridization (FISH).
Affiliations: Department of Clinical Laboratory, Hubei Maternal and Child Health Hospital, Wuhan, Hubei, People's Republic of China., Department of Clinical Laboratory, Renmin Hospital Wuhan University, Wuhan, Hubei, People's Republic of China., Internal Medicine-Cardiovascular Department, Xiaogan Hospital affiliated to Wuhan University of Science and Technology, Xiaogan, Hubei, People's Republic of China.

Abstract:  The frequency of the Robertonian (ROB) translocation in newborn babies is approximately one in 1000. Robertsonian translocation is an unusual type of chromosome rearrangement caused by two particular chromosomes joining together. The aim of the study was to analyze the segregation of the ROB translocations in 13 male carriers, and to verify a possible inter-chromosomal effect (ICE) of the ROB translocation on chromosomes 18, X, and Y. Thirteen male patients were included in the study. Multicolor fluorescent in situ hybridization (FISH) was used to analyze chromosomes 13, 14, 15, 21, 22, 18, X and Y in sperm. Among the heterozygous ROB translocation carriers, the frequency of normal/balanced spermatozoa resulting from alternate segregation varied between 70.4 and 85.2%. The frequency of unbalanced spermatozoa resulting from adjacent segregation varied between 14.8 and 29.6%. Increased frequencies of aneuploidy for a sex chromosome were found in 10 ROB translocation carriers (P2-P8, P10-P12). Increased frequencies of aneuploidy for chromosome 18 were found in10 ROB translocation carriers (P3-P9, P11-P13). In addition, increased frequencies of diploid were found in 11 ROB translocation carriers (P2-P9, P11-P13). Among the homozygous ROB translocation carriers, the rate of balanced spermatozoa was 99.7% and the frequency of unbalanced spermatozoa was 0.3%. However, the frequencies of aneuploidy for a sex chromosome and chromosome 18 were normal. Despite the high number of normal/balanced frequencies, there remained many unbalanced spermatozoa resulting from alternate segregation. The ROB translocation carriers may be at an increased risk for ICE. Robertsonian translocation homozygosity could be seen as a potential speciation in humans with 44 chromosomes. 

Retracted: No

PubPeer comments:
 The authors use several figures and data from their previous paper (Song et al., Molecular Cytogenetics 2016; 9:48) in this publication without acknowledgement or citation. All figures and data reproduced from previous publications must be properly cited. ![file] ![file] ![file] ,
The marine‐derived furanone reduces intracellular lipid accumulation in vitro by targeting LXRα and PPARα
Authors: Bin Xia
Fa-Hui Li
Shu-Mei Hu
Jia-Yu Yin
Xiao-Qian Yang
Jun-Feng Wang
Ting Li
Xiao-Yan Pang
Wei-Guo Song
Shou-Dong Guo
Jin Wang
Yong-Hong Liu
Journal: Journal of Cellular and Molecular Medicine (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LXR antagonist; PPAR antagonist; PPARα agonist; acetyl-CoA carboxylase; fatty acid synthase
Affiliations: Institute of Lipid Metabolism and Atherosclerosis, School of Pharmacy, Innovative Drug Research Centre, Weifang Medical University, Weifang, China., CAS Key Laboratory of Tropical Marine Bio-resources and Ecology/Guangdong Key Laboratory of Marine Materia Medica/RNAM Center for Marine Microbiology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China.

Abstract:  Recent studies have demonstrated that commercially available lipid-lowering drugs cause various side effects; therefore, searching for anti-hyperlipidaemic compounds with lower toxicity is a research hotspot. This study was designed to investigate whether the marine-derived compound, 5-hydroxy-3-methoxy-5-methyl-4-butylfuran-2(5H)-one, has an anti-hyperlipidaemic activity, and the potential underlying mechanism in vitro. Results showed that the furanone had weaker cytotoxicity compared to positive control drugs. In RAW 264.7 cells, the furanone significantly lowered ox-LDL-induced lipid accumulation (~50%), and its triglyceride (TG)-lowering effect was greater than that of liver X receptor (LXR) agonist T0901317. In addition, it significantly elevated the protein levels of peroxisome proliferator-activated receptors (PPARα) and ATP-binding cassette (ABC) transporters, which could be partially inhibited by LXR antagonists, GSK2033 and SR9243. In HepG2 cells, it significantly decreased oleic acid-induced lipid accumulation, enhanced the protein levels of low-density lipoprotein receptor (LDLR), ABCG5, ABCG8 and PPARα, and reduced the expression of sterol regulatory element-binding protein 2 (~32%). PPARα antagonists, GW6471 and MK886, could significantly inhibit the furanone-induced lipid-lowering effect. Furthermore, the furanone showed a significantly lower activity on the activation of the expression of lipogenic genes compared to T0901317. Taken together, the furanone exhibited a weak cytotoxicity but had powerful TC- and TG-lowering effects most likely through targeting LXRα and PPARα, respectively. These findings indicate that the furanone has a potential application for the treatment of dyslipidaemia. 

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. ,
Molecular characterization of Legionella pneumophila-induced interleukin-8 expression in T cells
Authors: Jiro Fujita
Reika Takamatsu
Jian-Dong Li
Futoshi Higa
Eriko Takeshima
Kunihiro Matsumoto
Hiromitsu Teruya
Chie Ishikawa
Naoki Mori
Naofumi Mukaida
Klaus Heuner
Journal: BMC Microbiology (2010)
Discipline: MICROBIOLOGY
Keywords: Legionella pneumophila; T cells; IL-8; infection; immune system
Affiliations: Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.

Abstract:  Background: Legionella pneumophila is the causative agent of human Legionnaire's disease. During infection, the bacterium invades macrophages and lung epithelial cells, and replicates intracellularly. However, little is known about its interaction with T cells. We investigated the ability of L. pneumophila to infect and stimulate the production of interleukin-8 (IL-8) in T cells. The objective of this study was to assess whether L. pneumophila interferes with the immune system by interacting and infecting T cells. Results: Wild-type L. pneumophila and flagellin-deficient Legionella, but not L. pneumophila lacking a functional type IV secretion system Dot/Icm, replicated in T cells. On the other hand, wild-type L. pneumophila and Dot/Icm-deficient Legionella, but not flagellin-deficient Legionella or heat-killed Legionella induced IL-8 expression. L. pneumophila activated an IL-8 promoter through the NF-kappaB and AP-1 binding regions. Wild-type L. pneumophila but not flagellin-deficient Legionella activated NF-kappaB, p38 mitogen-activated protein kinase (MAPK), Jun N-terminal kinase (JNK), and transforming growth factor beta-associated kinase 1 (TAK1). Transfection of dominant negative mutants of IkappaBalpha, IkappaB kinase, NF-kappaB-inducing kinase, TAK1, MyD88, and p38 MAPK inhibited L. pneumophila-induced IL-8 activation. Inhibitors of NF-kappaB, p38 MAPK, and JNK blocked L. pneumophila-induced IL-8 expression. In addition, c-Jun, JunD, cyclic AMP response element binding protein, and activating transcription factor 1, which are substrates of p38 MAPK and JNK, bound to the AP-1 site of the IL-8 promoter. Conclusions: Taken together, L. pneumophila induced a flagellin-dependent activation of TAK1, p38 MAPK, and JNK, as well as NF-kappaB and AP-1, which resulted in IL-8 production in human T cells, presumably contributing to the immune response in Legionnaire's disease. 

Retracted: No

PubPeer comments:
 Retracted 2 June 2011. Retraction notice: https: bmcmicrobiol.biomedcentral.com articles 10.1186 1471-2180-11-127 It reads:  After lengthy investigation by the editors, the original article [1] has been retracted because of inappropriate duplication of images from previously published articles. The last author, Naoki Mori takes full responsibility and apologizes for any inconvenience caused. During a 2015 post-mortem analysis, Figure 2B appeared to show two b-actin panels that look very similar. ![file] In addition, b-actin panels in Figure 2A and Figure 3B also looked unexpectedly similar. I did not check for more. ![file] ,
EGFR Targeted Paclitaxel and Piperine Co-loaded Liposomes for the Treatment of Triple Negative Breast Cancer
Authors: Abhishek Jha
Sanjeev Kumar Mahto
Azad Shaik
Madaswamy S Muthu
Ankita Sanjay Burande
Abhishesh Kumar Mehata
Suruchi Poddar
Nishi Agrawal
Matte Kasi Viswanadh
Journal: AAPS PharmSciTech (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: breast cancer; cetuximab; liposomes; paclitaxel; piperine.
Affiliations: Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (BHU), Varanasi, 221005, India., School of Biomedical Engineering, Indian Institute of Technology (BHU), Varanasi, 221005, India., Centre for Biomaterials and Tissue Engineering, Indian Institute of Technology (BHU), Varanasi, 221005, India., Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (BHU), Varanasi, 221005, India. ., Centre for Biomaterials and Tissue Engineering, Indian Institute of Technology (BHU), Varanasi, 221005, India. .

Abstract:  Triple-negative breast (TNBC) cancer that is upregulated with epidermal growth factor receptor (EGFR), and devoid of both the hormonal receptors and epidermal growth factor receptor 2 (HER 2), has led to a concept of treating TNBC with EGFR-targeted therapeutics. The combination of paclitaxel (PTX) and piperine (PIP) may improve the bioavailability of paclitaxel for cancer therapy. TPGS (vit E-PEG 1000-succinate)-coated liposomes were prepared with PTX alone or in combination with PIP, and either with (targeted) or without (non-targeted) cetuximab (CTX) conjugation. The Bradford assay indicated that 75% of CTX has been conjugated on the liposomes. The size and percent encapsulation of PTX&amp;PIP co-loaded liposomes were found to be in the range of 204 to 218 nm and 31-73%, respectively. The drug release rate was found to be higher at pH 5.5 in comparison with release at pH 6.4 and pH 7.4. Cellular uptake and toxicity studies on MDA-MB-231 cells showed that PTX&amp;PIP co-loaded targeted liposomes have demonstrated superior uptake and cytotoxicity than their non-targeted counterparts. The IC50 values of both of the liposomal formulations were found to be significantly higher than PTX control. Indeed, combining PIP with PTX control has improved the cytotoxicity of PTX control, which proved the synergistic anticancer effect of PIP. Lyophilized liposomes showed an excellent stability profile with the size range between 189 and 210 nm. Plasma stability study revealed a slight increase in the particle size due to the adsorption of plasma proteins on the surface of liposomes. The long-term stability study also indicated that liposomes were stable at 4°C. 

Retracted: No

PubPeer comments:
 The connection is strong. Wuhan coronavirus CRISPR. The intention of this [paper is good] - but CRISPR would integrate in the virus, as it did here for [HBV] in this 2014 paper. We need to start accepting what data tells us. [Ignoring] it for the hype does not help. ,