PReD-Bench/PRed-Bench huggingface dataset:
Cerebrospinal fluid atypical lymphocytes in Japanese encephalitis
Authors: H Kuno
N Hachiya
Y Sato
K Oizumi
T Asoh
Journal: Journal of the Neurological Sciences (1998)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Atypical lymphocytes; CD4+; CD8+; Encephalitis; Cerebrospinal fluid

Abstract:  Among atypical lymphocytes (AL) examined morphologically and immunohistochemically in the cerebrospinal fluid (CSF) of adult patients with encephalitis, we distinguished a CD4+ 'type I' AL, with a multilobulated nucleus resembling those of the abnormal cells in adult T-cell leukemia (ATL), from a CD8+ 'type II' AL, a large lymphocyte with basophilic cytoplasm and a nucleus containing coarse chromatin. Type I AL were detected in 7 of 8 patients with Japanese encephalitis (JE), but in none of 11 patients with herpes simplex encephalitis (HSE) and none of 19 patients with unspecified acute viral encephalitis. Type II AL were seen frequently in all three groups. The observation of type I AL in CSF strongly suggests JE, which warrants careful follow-up without antiherpetic drugs. In identifying type I AL, which presumably are virally transformed lymphocytes, care must be taken to distinguish them from leukemic involvement by ATL cells, which frequently includes the meninges. Both type I and type II AL also must be differentiated from lymphoma cells. 

Retracted: No

PubPeer comments:
 This paper should be retracted. There is a context of multiple ( 90) retractions of work by this group of researchers for a wide range of reasons that include fabrication, authorship misconduct, duplicate data reporting, plagiarism, unethical research practices, unresolved concerns about data integrity and scientific misconduct (http: retractionwatch.com the-retraction-watch-leaderboard ). The journal and its publisher were notified about the concerns with this paper in late 2018 early 2019 by Kurume University and by our group in July 2019 Concerns Ethical oversight The study was conducted by staff affiliated to Futase Hospital and Kurume University School of Medicine. It was reported to be approved by the u201cHuman Investigation Committee at our hospitalu2019 However, recent retractions of papers by Dr Sato and colleagues by Stroke and Bone indicate that neither Futase Hospital nor Kurume University Medical Center had an ethics committee at the time the work reported in this paper was supposedly conducted. Thus, this work is unethical. Authorship Kurume University concluded in late 2018 that this work should be retracted because of u2018malpractice: inappropriate authorshipu2019 , 
 On June 14 2020, the publisher informed us that this paper was to be retracted. 9 months later it has not been. Lengthy delays in publishing retraction notices is not in the best interest of readers. , 
 It is now 21 months since Elsevier communicated, via COPE, its undertaking to retract this paper. Recent requests for an update on the retraction to Elsevier, COPE, and the journal did not receive a response. The society associated with the journal, the World Federation of Neurology, responded but was unable to provide any information. ,
Acidotoxicity and acid-sensing ion channels contribute to motoneuron degeneration
Authors: A T Behan
M Mitchem
K Coughlan
J H M Prehn
B Breen
M Hogg
I Woods
Journal: Cell death and differentiation (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Amyotrophic lateral sclerosis (ALS); Mitochondrial dysfunction; Ca(2+) overloading; Hypoxic/ischemic environments; Metabolic acidosis
Affiliations: Department of Physiology and Medical Physics, Centre for the Study of Neurological Disorders, Royal College of Surgeons In Ireland, 123 St. Stephen's Green, Dublin, Ireland.

Abstract:  Amyotrophic lateral sclerosis (ALS) is a fatal neurological condition with no cure. Mitochondrial dysfunction, Ca(2+) overloading and local hypoxic/ischemic environments have been implicated in the pathophysiology of ALS and are conditions that may initiate metabolic acidosis in the affected tissue. We tested the hypothesis that acidotoxicity and acid-sensing ion channels (ASICs) are involved in the pathophysiology of ALS. We found that motoneurons were selectively vulnerable to acidotoxicity in vitro, and that acidotoxicity was partially reduced in asic1a-deficient motoneuron cultures. Cross-breeding of SOD1(G93A) ALS mice with asic1a-deficient mice delayed the onset and progression of motor dysfunction in SOD1 mice. Interestingly, we also noted a strong increase in ASIC2 expression in motoneurons of SOD1 mice and sporadic ALS patients during disease progression. Pharmacological pan-inhibition of ASIC channels with the lipophilic amiloride derivative, 5-(N,N-dimethyl)-amiloride hydrochloride, potently protected cultured motoneurons against acidotoxicity, and, given post-symptom onset, significantly improved lifespan, motor performance and motoneuron survival in SOD1 mice. Together, our data provide strong evidence for the involvement of acidotoxicity and ASIC channels in motoneuron degeneration, and highlight the potential of ASIC inhibitors as a new treatment approach for ALS. 

Retracted: Yes

PubPeer comments:
 undeclared slice site of immunoblot in Fig.5D. ![file] ,
Role of intergenic sequences in newcastle disease virus RNA transcription and pathogenesis
Authors: Yongqi Yan
Siba K Samal
Journal: Journal of virology (2008)
Discipline: MICROBIOLOGY
Keywords: Newcastle disease virus; IGS length; transcription; pathogenesis; deletion
Affiliations: Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, 8075 Greenmead Drive, College Park, MD 20742, USA. , Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, Maryland 20742

Abstract:  Newcastle disease virus (NDV), a member of the family Paramyxoviridae, has a nonsegmented negative-sense RNA genome consisting of six genes (3'-NP-P-M-F-HN-L-5'). The first three 3'-end intergenic sequences (IGSs) are single nucleotides (nt), whereas the F-HN and HN-L IGSs are 31 and 47 nt, respectively. To investigate the role of IGS length in NDV transcription and pathogenesis, we recovered viable viruses containing deletions or additions in the IGSs between the F and HN and the HN and L genes. The IGS of F-HN was modified to contain an additional 96 nt or more or a deletion of 30 nt. Similarly, the IGS of HN-L was modified to contain an additional 96 nt or more or a deletion of 42 nt. The level of transcription of each mRNA species (NP, F, HN, and L) was examined by Northern blot analysis. Our results showed that NDV can tolerate an IGS length of at least 365 nt. The extended lengths of IGSs down-regulated the transcription of the downstream gene and suggested that 31 nt in the F-HN IGS and 47 nt in the HN-L IGS are required for efficient transcription of the downstream gene. The effect of IGS length on pathogenicity of mutant viruses was evaluated in embryonated chicken eggs, 1-day-old chicks, and 6-week-old chickens. Our results showed that all IGS mutants were attenuated in chickens. The level of attenuation increased as the length of the IGS increased. Interestingly, decreased IGS length also attenuated the viruses. These findings can have significant applications in NDV vaccine development. 

Retracted: No

PubPeer comments:
 February 2020 correction, which reads:  Figure 4: Due to an error in figure assembly, plaque morphology of rBC-FHNu039430 (top row, 3rd column) and rBC-HNLu039430 (2nd row from the top, 3rd column) are inadvertent duplicate images. The Fig. 4 panels showing plaque morphology of rBC-FHNu039430 and rBC-HNLu039430 should appear as shown below. (...) Correction of this image does not change the interpretation of results or the conclusions of the paper. PUBLISHERu2019S NOTE The University of Marylandu2019s investigation determined these to be u201chonest error.u201d Here is the original Figure 4, with the duplication marked in red. ![file] ,
LncRNA MNX1‐AS1 promotes the progression of cervical cancer through activating MAPK pathway
Authors: Xiahui Zhang
Meiyun Zheng
Xiang Liu
Jinyu Yan
Qian Yang
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MAPK pathway.; MNX1-AS1; apoptosis; cervical cancer; proliferation.
Affiliations: Department of Obstetrics and Gynecology, The First People's Hospital of Wenling, Wenling, Zhejiang, China.

Abstract:  Long noncoding RNAs (lncRNAs) have been discovered as significant regulators in a wide range of human cancers. Among them, lncRNA MNX1-AS1 has been proved to be an oncogene in ovarian cancer and glioblastoma. However, the regulatory mechanism of MNX1-AS1 in cervical cancer remains to be understood. Therefore, this study planned to explore the role of MNX1-AS1 in cervical cancer. In the beginning, we found that the expression of MNX1-AS1 was obviously upregulated in cervical cancer tissues and cell lines. Kaplan-Meier survival analysis revealed that patients with higher MNX1-AS1 expression level suffered from shorter overall survival time than those with lower MNX1-AS1 level. Moreover, by loss-of-function and gain-of-function assay, the effect of MNX1-AS1 on cell proliferation and apoptosis was examined on cellular level. Results showed that the proliferation of Hela cells was significantly inhibited and apoptosis enhanced by the transfection of shMNX1-AS1, while overexpressing MNX1-AS1 in E6E7 cells presented the contrary results. As for mechanism investigation, it was demonstrated that overexpression of MNX1-AS1 significantly improved the expression of p-ERK1/2 and p-JNK. And the effects of MNX1-AS1 on cell proliferation and apoptosis would be diminished after inactivating the phosphorylation of either ERK or JNK. Taken together, it was identified that MNX1-AS1 promoted proliferation and inhibited apoptosis of cervical cancer cells through MAPK pathway. 

Retracted: No

PubPeer comments:
 Figure 4A. * Remarkable similar regions shared among four different flow cytometry plots ![file] , 
 Could the authors please clarify during which period (which months years) the patients were recruited? ,
Hepatocyte nuclear factor-1 beta protects endometriotic cells against apoptotic cell death by up-regulating the expression of antiapoptotic genes†
Authors: Youn Seok Choi
Jung-Hye Choi
Umma Hafsa Preya
Jeong-Hwa Woo
Journal: Biology of Reproduction (2019)
Discipline: CLINICAL MEDICINE
Keywords: HNF1β; NF-κB; antiapoptotic gene; apoptosis; endometriosis
Affiliations: College of Pharmacy, Kyung Hee University, Seoul, South Korea., Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, South Korea., Department of Obstetrics and Gynecology, School of Medicine, Catholic University of Daegu, Daegu, South Korea.

Abstract:  The overexpression of hepatocyte nuclear factor-1 beta (HNF1β) in endometriotic lesion has been demonstrated. However, the role of HNF1β in endometriosis remains largely unknown. Human endometriotic 12Z cells showed higher level of HNF1β when compared with normal endometrial HES cells. In human endometriotic 12Z cells, HNF1β knockdown increased susceptibility to apoptotic cell death by oxidative stress, while HNF1β overexpression suppressed apoptosis. In addition, HNF1β knockdown and overexpression significantly decreased and increased, respectively, the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-dependent antiapoptotic genes. Knockdown of the antiapoptotic genes significantly reduced the HNF1β-induced resistance against oxidative stress in 12Z cells. Furthermore, HNF1β regulated the transcriptional activity of NF-κB, and an NF-κB inhibitor suppressed the HNF1β-enhanced NF-κB-dependent antiapoptotic gene expression and the resistance of the 12Z cells against cell death. Taken together, these data suggest that HNF1β overexpression may protect endometriotic cells against oxidative damage by augmenting antiapoptotic gene expression. 

Retracted: No

PubPeer comments:
 One of the cells used in this paper is described as such: * The human normal endometrial cells (HES cells) were kindly provided by Dr. Asgi Fazleabas (Michigan State University, East Lansing, MI, USA). * It is possible that the HES cells provided by Asgi Fazleabas are identical to the HES cell line which is not a normal endometrial cell line, but was later shown, by the group that established it [PMID:24520087] to be contaminated by the WISH cell line which is itself contaminated by HeLa. We believe that this may be the case because the group of Fazleabas has indicated in some papers like [PMID:19556419] to have used the  HES cells (a generous gift from Dr. Douglas Kniss, Ohio State University, Columbus, OH) Thus if the HES cells in this paper correspond to the HES cell line, some results may be affected by the use of this contaminated cell line. See the relevant Cellosaurus entries: [HES] and [WISH] ,
WITHDRAWN: COVID-19, its novel vaccination and fake news – What a brew
Authors: Victor Grech
Mariella Scerri
Journal: Early Human Development (2020)
Discipline: CLINICAL MEDICINE
Keywords: Article withdrawal; Author; Editor; Publisher; Elsevier Policy
Affiliations: Mater Dei Hospital, Malta. Electronic address: .

Abstract:  This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal. 

Retracted: No

PubPeer comments:
 **Withdrawn** in March, 2021: https: doi.org 10.1016 j.earlhumdev.2020.105256  *This article has been withdrawn at the request of the author(s) and or editor. The Publisher apologizes for any inconvenience this may cause.* *The full Elsevier Policy on Article Withdrawal can be found at https: www.elsevier.com about our-business policies article-withdrawal.* The background of this withdrawal has been covered by Retraction Watch: https: retractionwatch.com 2021 03 31 beam-us-up-elsevier-pulls-26-covid-19-papers-by-researcher-with-a-penchant-for-star-trek ,
Peptide utilizing carbon starvation gene yjiY is required for flagella mediated infection caused by Salmonella
Authors: Dipshikha Chakravortty
Dipan Ghosh
Jayanta Chatterjee
Amit Lahiri
Preeti Garai
Journal: Microbiology (2016)
Discipline: MICROBIOLOGY
Keywords: Peptide metabolism; Salmonella; peptide transporters; carbon starvation genes; cstA
Affiliations: Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India., Molecular Biophysics Unit, Indian Institute of Science, Bangalore, India.

Abstract:  Peptide metabolism forms an important part of the metabolic network of Salmonella and to acquire these peptides the pathogen possesses a number of peptide transporters. While various peptide transporters known in Salmonella are well studied, very little is known about the carbon starvation (cst) genes, cstA and yjiY, which are also predicted to be involved in peptide metabolism. We investigated the role of these genes in the metabolism and pathogenesis of Salmonella and demonstrated for the first time that cst genes actually participate in transport of specific peptides in Salmonella. Further, we established that the carbon starvation gene yjiY affects the expression of flagella leading to poor adhesion of the bacterium to host cells. In contrast with the previously reported role of the gene cstA in virulence of Salmonella in C. elegans, we showed that yjiY is required for successful colonization of Salmonella in the mouse gut. Thus, cst genes not only contribute to the metabolism of Salmonella but also influence its virulence. 

Retracted: No

PubPeer comments:
 ![file] , 
 Dear reader,u00a0 Thank you for making the observation. The panel for yjiY KO-pTrc-fliC was repeated by mistake. We are attaching the corrected version containing the panel yjiYu00a0KO-pQE60-yjiY . We hope this satisfies your query. Thank you, Preeti Garai ![file] ,
MicroRNA-187, a downstream effector of TGFβ pathway, suppresses Smad-mediated epithelial–mesenchymal transition in colorectal cancer
Authors: Jiaolong Shi
Yuhao Luo
Ya Niu
Xuegang Sun
Xiaoxu Liu
Yanqing Ding
Lijun Xu
Feifei Zhang
Liang Zhao
Ziyun Shao
Yawei Liu
Journal: Cancer Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: Colorectal carcinoma; Epithelial–mesenchymal transition; Transforming growth factor beta; Tumor metastasis; microRNA-187.
Affiliations: Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China., The Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine; School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China., Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China., Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. Electronic address: .

Abstract:  Constitutive overactivation of TGFβ signaling is a common event in human cancer progression and acts as a major inducer of epithelial-mesenchymal transition (EMT). In pre-metastatic colorectal cancer (CRC) cells, however, this cascade is tightly controlled and the underlying mechanism in TGFβ stimulated hyperactivation of downstream Smad pathway remains elusive. In this study, expression of miR-187 was downregulated in colorectal cancer (CRC) compared with adjacent normal tissues. miR-187 could suppress the formation of aggressive phenotype in CRC and inactivate Smad pathway, thus preventing EMT. TGFβ stimulation significantly suppressed the expression of miR-187, and overexpressed miR-187 counteracted the influence of TGFβ on cell phenotype and downstream pathway. Furthermore, we found that miR-187 directly suppressed the expression of SOX4, NT5E and PTK6, which were identified as essential upstream effectors of Smad pathway. Together with the fact that high SOX4 or NT5E levels were associated with poor prognosis, we also demonstrated that downregulation of miR-187 was closely related to tumor metastasis and poor prognosis in CRC. These findings revealed a plausible mechanism for sustained TGFβ activation in cancer progression and might have suggested a novel miR-187-based clinical intervention target for patients with advanced CRC. 

Retracted: No

PubPeer comments:
 The nanoparticles presented in Figure 2 are too perfect and the white halo effect around them looks odd. ![file] ,
CD80 in Immune Suppression by Mouse Ovarian Carcinoma–Associated Gr-1+CD11b+ Myeloid Cells
Authors: Katherine F Roby
Yuan Zhang
Zhong Cai
Rongcun Yang
Richard B S Roden
William H Yutzy 4th
Journal: Cancer Research (2006)
Discipline: CLINICAL MEDICINE
Keywords: Gr-1+CD11b+ myeloid cells; immune suppression; ovarian carcinoma; CD80 expression; CD40
Affiliations: Department of Immunology, College of Medicine, Nankai University, Tianjin, China. 

Abstract:  An elevated number of Gr-1+CD11b+ myeloid cells has been described in mice bearing transplantable tumors, and has been associated with immune suppression. We examined the role of such myeloid suppressor cells in mice bearing the spontaneously transformed syngeneic mouse ovarian surface epithelial cell line, 1D8. We observed high levels of CD80 expression by Gr-1+CD11b+ cells from spleen, ascites, and tumor tissue of mice bearing 1D8 ovarian carcinoma, whereas CD40 and CD86 were absent. CD80 expression was not detected on Gr-1+CD11b+ cells from naïve mice. However, the expression of CD80 by Gr-1+CD11b+ cells from naïve mice was promoted by coculture with 1D8 cells. Because irradiated 1D8 cells, but not 1D8-conditioned medium, up-regulate CD80 expression by Gr-1+CD11b+ cells, this phenomenon likely requires direct interaction. Gr-1+CD11b+ cells derived from 1D8 tumor-bearing mice provided significant suppression of antigen-specific immune responses, but Gr-1+CD11b+ cells from naïve mice did not. Both short interfering RNA-mediated knockdown and genetic knockout of CD80 expression by Gr-1+CD11b+ cells of 1D8 tumor-bearing mice alleviated the suppression of antigen-specific immune responses. Suppression via CD80 on Gr-1+CD11b+ myeloid cells was mediated by CD4+CD25+ T regulatory cells and required CD152. CD80 knockout or antibody blockade of either CD80 or CD152 retarded the growth of 1D8 tumor in mice, suggesting that expression of CD80 on Gr-1+CD11b+ myeloid cells triggered by 1D8 ovarian carcinoma suppresses antigen-specific immunity via CD152 signaling and CD4+CD25+ T regulatory cells. Thus, CD80-dependent responses to myeloid suppressor cells may contribute to tumor tolerance and the progression of ovarian carcinoma. 

Retracted: No

PubPeer comments:
 Dear authors, I find that some flow images are having unexpected similarities on fig 1![file] ![file] ,
Up-regulated lncRNA GAS5 promotes chemosensitivity and apoptosis of triple-negative breast cancer cells
Authors: Xing-Wei Huang
Juntao Li
Sujuan Dai
Lin Li
Huozhong Yuan
Tianxin Xiang
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GAS5; methylation; triple-negative breast cancer.
Affiliations: a Departmnet of Breast and Thyroid Surgery, People's Hospital of Ganzhou City , Ganzhou , Jiangxi Province , PR. China., b Departmnet of Pharmacy Intravenous Admixture Services, People's Hospital of Ganzhou City , Ganzhou , Jiangxi Province , PR. China., c Department of Infectious Diseases, The First Affiliated Hospital of Nanchang Universicty , Nanchang , Jiangxi Province , PR. China., d Departmnet of Pathology, People's Hospital of Ganzhou City , Ganzhou , Jiangxi Province , PR. China.

Abstract:  Up to accomplishment of this study, the role of long non-coding RNAs (lncRNAs) in breast cancer has been investigated in several researches. Nevertheless, its association with the chemosensitivity of cancer was little known. Therefore, this study is focused on lncRNA GAS5 and its influence in the chemosensitivity of triple-negative breast cancer (TNBC). Expression of GAS5 in TNBC tissues and cells was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and its methylation was evaluated using methylation-specific polymerase chain reaction (MSP). Moreover, in order to define the contributory role of GAS5 in TNBC, GAS5 expression, proliferation, and apoptosis of TNBC cells were detected by a series of experiment. Finally, the effects of GAS5 in vivo were investigated by measuring tumor formation in nude mice. GAS5 was poorly expressed in TNBC tissues and cells, which could regulate the progression of TNBC. The methylation of CpG island in the promoter region of GAS5 in MDA-MB-231 and MDA-MB-468 cells was decreased, while GAS5 expression in cells was increased. Overexpressed GAS5 reduced the inhibitory concentration (IC50) value and the cell proliferation of TNBC, and promoted their apoptosis, so as to delay the progression of TNBC. Our study provides evidence that up-regulated GAS5 suppressed the progression of TNBC and promoted chemosensitivity and apoptosis of TNBC cells. Thus, GAS5 may be a potential candidate for the treatment of TNBC. 

Retracted: No

PubPeer comments:
 Figure 5E and Figure 5F. Much more similar than expected. ![file] ,
Proteome changes associated with Leishmania donovani promastigote adaptation to oxidative and nitrosative stresses
Authors: Pradeep Das
Sudeep Kumar
Kislay Kumar Sinha
Manish Kumar
Dharmendra Singh
Asif Equbal
Abul Hasan Sardar
Sushmita Das
Abhik Sen
Bidyut Purkait
Vahab Ali
Ashish Kumar
Journal: Journal of Proteomics (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Phagocytic cells; reactive oxygen species; nitrogen species; Leishmania; proteome
Affiliations: Division of Molecular Biology, Rajendra Memorial Research Institute of Medical Sciences, Agamkuan, Patna-800007, Bihar, India.

Abstract:  Phagocytic cells produce reactive oxygen and nitrogen species (ROS &amp; RNS) as the most common arsenal to kill intracellular pathogens. Leishmania, an obligate intracellular pathogen also confronts this antimicrobial assault during the early phase of infection but nevertheless is able to survive these attacks and proliferate in macrophage. Adaptation of Leishmania to the toxic effects of ROS and RNS, involves a rapid change in the parasite proteome to combat the host defense response that macrophage mount in combating pathogen. To understand the events associated with combating ROS and RNS species, we performed a proteomic analysis of L. donovani promastigotes treated with sub-lethal doses of menadione (ROS), S-nitroso-N-acetylpenicillamine (RNS) or combination of both compounds. Proteomic changes triggered by these reagents were evaluated by iTRAQ labeling and subsequent LC-MALDI-TOF/TOF-MS analysis. Across the 3 stress conditions, the quantitative analysis identified changes in the proteins which encompass ~20% of the parasite proteome. Major changes were observed in enzymatic machinery of pathways involved in maintaining redox homeostasis, trypanothione metabolism, oxidative phosphorylation, superoxide metabolism, mitochondrial respiration process and other essential metabolic pathways. These observations shed light on how Leishmania promastigotes counter ROS and RNS effects during the initial stage of infection. This article is part of a Special Issue entitled: From protein structures to clinical applications. 

Retracted: No

PubPeer comments:
 Concern about Figure 5A. * Red boxes: All seven timepoints appear to have the same a-tubulin band. ![file] , 
 Concern about Figure 8: * Several bands appear to look more similar to each other than expected, albeit representing different proteins or experiments. ![file] ,
Synthesis of Vitamin B12-Antibiotic Conjugates with Greatly Improved Activity against Gram-Negative Bacteria
Authors: Zhi-Peng Wang
Guoxing Wei
Xumei Wen
Sheng Zhao
Yun He
Jian Guo
Siyu Li
Journal: Organic Letters (2020)
Discipline: CHEMISTRY
Keywords: antibiotics; Gram-negative bacteria; Trojan horse conjugates; vitamin-B12; ampicillin
Affiliations: Chongqing Key Laboratory of Natural Product Synthesis and Drug Research, School of Pharmaceutical Sciences, Chongqing University, Chongqing 401331, P.R. China, Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing 400714, China

Abstract:  There is an urgent need to discover new antibiotics and improve the efficacy of known antibiotics against Gram-negative bacteria. "Trojan horse" conjugates are novel and promising antibiotics. Herein we report the design and synthesis of vitamin-B12-ampicillin conjugates, which exhibited more than 500 times improved activity against Escherichia coli compared with ampicillin itself. Our studies demonstrate that the vitamin-B12 uptake pathway could be employed for effective antibiotic delivery and efficacy enhancement. 

Retracted: No

PubPeer comments:
 Fig 1.A. Does not at all represent the nutrient-based Trojan Horse Strategy (THS) - None of the transporters targeted by THS reported so far are based on such a  flip-flop transition - Transporters are not embedded in the cell wall but in the outer membrane in Gram-neg bacteria ,
LncRNA TDRG1 promotes the metastasis of NSCLC cell through regulating miR‐873‐5p/ZEB1 axis
Authors: Jiaojie Wang
Yu Mu
Xiufeng Hu
Yanqiu Zhao
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NSCLC; TDRG1; ZEB1; metastasis; miR-873-5p.
Affiliations: Department of RespiratoryAffiliated Cancer Hospital of Zhengzhou UniversityZhengzhou Henan China, Department of blood component preparationHenan Red Cross Blood CenterZhengzhou Henan China

Abstract:  Long noncoding RNAs (lncRNAs) are dysregulated in various malignancies and involved in the growth and aggressive phenotypes of cancer cells. Previous studies indicate that lncRNA testis development related 1 (TDRG1) plays critical roles in the development of several malignancies. Nevertheless, the molecular mechanism underlying TDRG1 contributes to non-small cell lung cancer (NSCLC) remains elusive. Here, we demonstrate that TDRG1 is significantly overregulated in NSCLC tissues and cell lines. Knockdown of TDRG1 inhibits the proliferation and metastatic-related traits of NSCLC cell in vitro whereas overexpression of TDRG1 causes opposite results. In addition, TDRG1 silencing inhibits the growth and metastatic ability of NSCLC cell in vivo as demonstrated by xenograft tumor model and lung metastasis model. The binding capacity of TDRG1 with miR-873-5p is demonstrated by bioinformatics prediction tool and luciferase reporter gene assay. Additional, the rescue experiments indicate that TDRG1 interacts with miR-873-5p and its expression is positively associated with the target of miR-873-5p, zinc finger e-box binding homeobox 1 (ZEB1). Altogether, lncRNA TDRG1 facilitates the progression of NSCLC via interacting with miR-873-5p and positively regulates the expression of ZEB1. 

Retracted: No

PubPeer comments:
 The micrographs in Figure 3B,D and Figure 6E have no background. Even if you push the contast to the extreme it is all white. Do the authors have any explanation? ![file] ,
Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis
Authors: Bastiaan Evers
Patrick W B Derksen
Jos Jonkers
Judy R van Beijnum
Jacqueline Vink
Hanneke van der Gulden
Paul Krimpenfort
Robert D Cardiff
Francis Saridin
John Zevenhoven
Xiaoling Liu
Anton Berns
Johannes L Peterse
Arjan W Griffioen
Journal: Cancer Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Metastatic disease; breast cancer; E-cadherin; invasive lobular carcinoma; p53
Affiliations: Division of Molecular Biology, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.

Abstract:  Metastatic disease is the primary cause of death in breast cancer, the most common malignancy in Western women. Loss of E-cadherin is associated with tumor metastasis, as well as with invasive lobular carcinoma (ILC), which accounts for 10%-15% of all breast cancers. To study the role of E-cadherin in breast oncogenesis, we have introduced conditional E-cadherin mutations into a mouse tumor model based on epithelium-specific knockout of p53. Combined loss of E-cadherin and p53 resulted in accelerated development of invasive and metastatic mammary carcinomas, which show strong resemblance to human ILC. Moreover, loss of E-cadherin induced anoikis resistance and facilitated angiogenesis, thus promoting metastatic disease. Our results suggest that loss of E-cadherin contributes to both mammary tumor initiation and metastasis. 

Retracted: No

PubPeer comments:
 Figure 2B. IRS-1 panels much more similar than you would expect even though the cells are different. https: imgur.com MVuduOq , 
 2020 correction. https: doi.org 10.1002 ijc.33274 u201cInsulin receptor substrate 1 is a target for the pure antiestrogen ICI 182,780 in breast cancer cells.u201d Salerno M, Sisci D, Mauro L, Guvakova MA, Ando S, Surmacz E. Int J Cancer. 1999, 81(2):299u2010304. In the Western Blot in Figure 2B of the aboveu2010mentioned manuscript, the bands for IRSu20101 in MCFu20107 IGFu2010IR and MCFu20107 cells look very similar. The authors are unable to retrieve the original data due to the time that has elapsed; therefore, duplication of the bands in question can neither be proven nor disproven. Given that the experiments presented in this manuscript have been performed in 1998 or earlier and logistic conditions are very different now, the editors consider that a reu2010performance of the experiments would not be appropriate. The authors stand by the conclusions of the paper. ,
Suppression of vascular permeability and inflammation by targeting of the transcription factor c-Jun
Authors: Alla Waldman
Michael Perry
Levon M Khachigian
Roger G Fahmy
Carolyn R Geczy
Colin N Chesterman
Guishui Zhang
Nicodemus Tedla
Ainslie Mitchell
Hong Cai
Journal: Nature Biotechnology (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: anti-inflammatory strategies; c-Jun; Dz13; vascular permeability; leukocytes
Affiliations: Centre for Vascular Research, University of New South Wales, and Department of Haematology, The Prince of Wales Hospital, Sydney NSW 2031, Australia.

Abstract:  Conventional anti-inflammatory strategies induce multiple side effects, highlighting the need for novel targeted therapies. Here we show that knockdown of the basic-region leucine zipper protein, c-Jun, by a catalytic DNA molecule, Dz13, suppresses vascular permeability and transendothelial emigration of leukocytes in murine models of vascular permeability, inflammation, acute inflammation and rheumatoid arthritis. Treatment with Dz13 reduced vascular permeability due to cutaneous anaphylactic challenge or VEGF administration in mice. Dz13 also abrogated monocyte-endothelial cell adhesion in vitro and abolished leukocyte rolling, adhesion and extravasation in a rat model of inflammation. Dz13 suppressed neutrophil infiltration in the lungs of mice challenged with endotoxin, a model of acute inflammation. Finally, Dz13 reduced joint swelling, inflammatory cell infiltration and bone erosion in a mouse model of rheumatoid arthritis. Mechanistic studies showed that Dz13 blocks cytokine-inducible endothelial c-Jun, E-selectin, ICAM-1, VCAM-1 and VE-cadherin expression but has no effect on JAM-1, PECAM-1, p-JNK-1 or c-Fos. These findings implicate c-Jun as a useful target for anti-inflammatory therapies. 

Retracted: No

PubPeer comments:
null, 
 Copy pasted from https: www.nature.com articles nbt0815-882c  Correction: Corrigendum: In the version of this article initially published, the first three bars in the histogram in Figure 1a should have read u201cNo vehicle,u201d u201cNo Dzu201d and u201cDz13u201d instead of u201cNo Dz,u201d u201cDz13u201d and u201cDz13scr.u201d The legend of Figure 1a should have included the sentences: u201c No vehicle represents the normoxia control without vehicle (transfection agent) or DNAzyme or siRNA. All other groups contain vehicle.u201d The H E-stained images in Figure 1a should have read u201cDz13 in hyperoxia-normoxiau201d and u201cDz13scr in hyperoxia-normoxiau201d instead of u201cNormoxiau201d and u201cHyperoxia-normoxia.u201d None of the conclusions is affected by the errors. The errors have been corrected in the HTML and PDF versions of the article. See for backgrounds also https: www.abc.net.au news 2019-10-17 unsw-skin-cancer-levon-khachigian-allegations-and-retractions 11585768 ,
Micro RNA ‐16 inhibits glioma cell growth and invasion through suppression of BCL 2 and the nuclear factor‐κB1/ MMP 9 signaling pathway
Authors: Yong-Xin Wei
Xiao-Jun Lu
Tian-Quan Yang
Zi-Wei Du
Zhao-Hui Zhao
Xue-Shun Xie
You-Xin Zhou
Yu-Lun Huang
Ling-Chuan Guo
Gui-Lin Chen
Da-Dong Ding
Bin Li
Ting-Feng Wu
Yu Zhang
Journal: Cancer Science (2014)
Discipline: CLINICAL MEDICINE
Keywords: BCL2; Glioma; MMP9; NF-κB1; miR-16.
Affiliations: Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China., Department of Neurosurgery The First People's Hospital of Tai Cang Suzhou China, Department of Neurosurgery and Brain and Nerve Research Laboratory The First Affiliated Hospital of Soochow University Suzhou China, Department of Pathology The First Affiliated Hospital of Soochow University Suzhou China

Abstract:  Recent studies have identified a class of small non-coding RNA molecules, named microRNA (miRNA), that is dysregulated in malignant brain glioblastoma. Substantial data have indicated that miRNA-16 (miR-16) plays a significant role in tumors of various origins. This miRNA has been linked to various aspects of carcinogenesis, including cell apoptosis and migration. However, the molecular functions of miR-16 in gliomagenesis are largely unknown. We have shown that the expression of miR-16 in human brain glioma tissues was lower than in non-cancerous brain tissues, and that the expression of miR-16 decreased with increasing degrees of malignancy. Our data suggest that the expression of miR-16 and nuclear factor (NF)-κB1 was negatively correlated with glioma levels. MicroRNA-16 decreased glioma malignancy by downregulating NF-κB1 and MMP9, and led to suppressed invasiveness of human glioma cell lines SHG44, U87, and U373. Our results also indicated that upregulation of miR-16 promoted apoptosis by suppressing BCL2 expression. Finally, the upregulation of miR-16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness. Taken together, our experiments have validated the important role of miR-16 as a tumor suppressor gene in glioma growth and invasiveness, and revealed a novel mechanism of miR-16-mediated regulation in glioma growth and invasiveness through inhibition of BCL2 and the NF-κB1/MMP-9 signaling pathway. Therefore, our experiments suggest the possible future use of miR-16 as a therapeutic target in gliomas. 

Retracted: No

PubPeer comments:
 Figure 4A. * Red boxes: Two panels appear to show an overlap. * Orange, purple, blue boxes: two panels appear to overlap with panels in Figure 2A of Hangzhou Wang et al., OncoTargets and Therapy (2015), 10.2147 OTT.S79282. See: https: pubpeer.com publications 7198830E465EBD70E334519FAD019B ![file] ,
Inhibition of cGAS-STING-TBK1 signaling pathway by DP96R of ASFV China 2018/1
Authors: Xiaoyu Guo
Shaohua Hou
Hongjun Chen
Jing Wu
Shoufeng Zhang
Ting Xin
Hongfei Zhu
Yingtong Wu
Yitong Jiang
Hong Jia
Jinxiang Li
Xixi Wang
Journal: Biochemical and biophysical research communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ASFV; DP96R; NF-κB; TBK1; Type I IFN
Affiliations: Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China., Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China; Gembloux Agro-bio Tech, University of Liège, Liège, 4000, Belgium., Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai 200241, China., Institute of Military Veterinary Medicine, Academy of Military Medical Sciences, Changchun 130000, China., Chinese Academy of Agricultural Sciences, Beijing 100081, China., Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China. Electronic address: .

Abstract:  African swine fever virus (ASFV) is a highly pathogenic large DNA virus that causes African swine fever (ASF) in domestic pigs and European wild boars with mortality rate up to 100%. The DP96R gene of ASFV encodes one of the viral virulence factors, yet its action mechanism remains unknown. In this study, we report that DP96R of ASFV China 2018/1 strain subverts type I IFN production in cGAS sensing pathway. DP96R inhibited the cGAS/STING, and TBK1 but not IRF3-5D mediated IFN-β and ISRE promoters activation. Furthermore, DP96R selectively blocked the activation of NF-κB promoter induced by cGAS/STING, TBK1, and IKKβ, but not by overexpression of p65. Moreover, DP96R inhibited phosphorylation of TBK1 stimulated by cGAS/STING activation, and TBK1-induced antiviral response. Finally, truncated mutation analysis demonstrated that the region spanning amino acids 30 to 96 of DP96R was responsible for the inhibitory activity. To our knowledge, this is for the first time that DP96R of ASFV China 2018/1 is reported to negatively regulate type I IFN expression and NF-κB signaling by inhibiting both TBK1 and IKKβ, which plays an important role in virus immune evasion. 

Retracted: No

PubPeer comments:
 The WB in Figure 1A appears to include some repeated elements (green boxes). Could the authors please provide the original uncropped scans? I did not look elsewhere. *** ![file] ,
Ponzo perspective illusion as a manifestation of space perception
Authors: R Brislin
R Hennessy
H Leibowitz
L Perlmutrer
Journal: Science (1969)
Discipline: Multidisciplinary
Keywords: Ponzo perspective illusion; space perception; contextual factors; texture; stereopsis

Abstract:  The Ponzo perspective illusion, a special case of space perception, is influenced by contextual factors, texture, stereopsis, and familiarity in addition to perspective cues. The importance of familiarity is demonstrated by cultural differences obtained with photographs of natural settings which emphasize depth cues. 

Retracted: No

PubPeer comments:
  Specifically, converging lines in the retinal image are ordinarily associated with distance and signal the organism to correct for the diminishing retinal image size of distant objects, that is, size constancy. This is actually not true as a general rule. Whether or not  converging lines will  signal distance depends on more global structural factors. Converging lines may appear fronto-parallel or as projecting forward, as well as projecting backward, depending on conditions. https: psyarxiv.com x2bsk ,
Src phosphorylation of Alix/AIP1 modulates its interaction with binding partners and antagonizes its activities
Authors: Ivan Dikic
Mirko Schmidt
Oliver Bögler
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Alix/AIP1; Src; adaptor protein; tyrosine kinases; SH2 domain
Affiliations: William and Karen Davidson Laboratory of Brain Tumor Biology, Hermelin Brain Tumor Center, Department of Neurosurgery, Henry Ford Hospital, Detroit, Michigan 48202, USA.

Abstract:  Alix/AIP1 is an adaptor protein involved in regulating the function of receptor and cytoskeleton-associated tyrosine kinases. Here, we investigated its interaction with and regulation by Src. Tyr319 of Alix bound the isolated Src homology-2 (SH2) domain and was necessary for interaction with intact Src. A proline-rich region in the C terminus of Alix bound the Src SH3 domain, but this interaction was dependent on the release of the Src SH2 domain from its Src internal ligand either by interaction with Alix Tyr319 or by mutation of Src Tyr527. Src phosphorylated Alix at a C-terminal region rich in tyrosines, an activity that was stimulated by the presence of the Alix binding partner SETA/CIN85. Phosphorylation of Alix by Src caused it to translocate from the membrane and cytoskeleton to the cytoplasm and reduced its interaction with binding partners SETA/CIN85, epidermal growth factor receptor, and Pyk2. As a consequence of this, Src antagonized the negative regulation of receptor tyrosine kinase internalization and cell adhesion by Alix. We propose a model whereby Src antagonizes the effects of Alix by phosphorylation of its C terminus, leading to the disruption of interactions with target proteins. 

Retracted: No

PubPeer comments:
 Figure 1E. https: imgur.com Vco7S0p , 
 Figure 2D. https: imgur.com 1n9dqwY ,
MicroRNA-143-5p targeting eEF2 gene mediates intervertebral disc degeneration through the AMPK signaling pathway
Authors: Qi Yang
Yang Wang
Xiao-Peng Guo
Yan-Li Cheng
Journal: Arthritis Research & Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: AMPK signaling pathway; Apoptosis; Differentiation; EEF2; MicroRNA-143-5p
Affiliations: The 3rd Ward of Department of Orthopedics Surgery, Taihe Hospital, Shiyan, 442000, People's Republic of China., Department of Dermatology, Taihe Hospital, Shiyan, 442000, People's Republic of China., The 2nd Ward of Department of Neurosurgery, Taihe Hospital, No. 32, Renmin South Road, Maojian District, Shiyan, 442000, Hubei Province, People's Republic of China. .

Abstract:  Background: Intervertebral disc degeneration (IDD) is a major contributor to back, neck, and radicular pain, and the treatment of IDD is costly and relatively ineffective. Dysregulation of microRNAs (miRNAs) has been reported to be involved in IDD. The purpose of our study is to illustrate the potential that miR-143-5p targeting eEF2 gene mediates IDD. Methods: Following the establishment of the IDD rat models, expression of miR-143-5p, eEF2, Bcl-2, Bax, AMPK, mTOR, cyclinD, COL2, ACAN, and DCN was detected. The NP cells isolated from degenerative intervertebral disc (IVD) were introduced with a series of mimic, inhibitor, or AICAR to explore the functional role of miR-143-5p in IDD and to characterize the relationship between miR-143-5p and eEF2. Cell viability, cell cycle, apoptosis, and senescence were also evaluated. Results: A reduction in eEF2, an increase in miR-143-5p, and activation of the AMPK signaling pathway were observed in degenerative IVD. Moreover, increased senescent NP cells were observed in degenerative IVD. eEF2 was confirmed as a target gene of miR-143-5p. miR-143-5p was found to activate the AMPK signaling pathway. The restoration of miR-143-5p or the activation of AMPK signaling pathway decreased COL2, ACAN, and DCN expression, coupled with the inhibition of NP cell proliferation and differentiation, and promotion of NP apoptosis and senescence. On the contrary, the inhibition of miR-143-5p led to the reversed results. Conclusion: The results demonstrated that the inhibition of miR-143-5p may act as a suppressor for the progression of IDD. 

Retracted: No

PubPeer comments:
 Fig 8b.  Cell cycles following treatment with miR-143-5p mimic, inhibitor or AICAR; AICAR was the activator of the AMPK signaling pathway; the experiment was repeated three times independently . ![file] These panels appear to have been hand-drawn, and do not make sense as flow-cytometry results. ,
N doped carbon coated V2O5 nanobelt arrays growing on carbon cloth toward enhanced performance cathodes for lithium ion batteries
Authors: Naiqing Zhang
Bingjiang Li
Yu Zhang
Pengxiang Wang
Lijun Wu
Lishuang Fan
Kening Sun
Journal: RSC Advances (2018)
Discipline: CHEMISTRY
Keywords: flexible; binder-free cathodes; lithium ion batteries; N doped carbon; V2O5
Affiliations: State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, PR China, Academy of Fundamental and Interdisciplinary Sciences

Abstract:  Highly flexible, binder-free cathodes for lithium ion batteries were fabricated by utilizing N doped carbon to coat V2O5 (V2O5@N-C) nanobelt arrays growing on carbon cloth. Such a robust architecture endows the electrode with effective ion diffusion and charge transport, resulting in high rate capability (135 mA h g-1 at 10C) and excellent cycling performance (215 mA h g-1 after 50 cycles at 0.5C). 

Retracted: No

PubPeer comments:
 Two identical XRD patterns , Fig.1 ![file] ,