PReD-Bench/PRed-Bench huggingface dataset:
Down-regulation of miR-206 is associated with Hirschsprung disease and suppresses cell migration and proliferation in cell models
Authors: Yankai Xia
Hua Xie
Ankur Sharan
Hairong Zhu
Hongwei Zhang
Junwei Tang
Weibing Tang
Hongxing Li
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: Hirschsprung disease; MiR-206; neural crest cells; qRT-PCR; Western blot
Affiliations: 1] Key Laboratory of Modern Toxicology (Nanjing Medical University), Ministry of Education, China [2] Department of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing 210008, China., 1] State Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China [2] Department of Pediatric Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing 210008, China., Department of Pediatric Surgery, Xuzhou Children's Hospital Affiliated to Xuzhou Medical University, Xuzhou 221002, China.

Abstract:  Hirschsprung disease (HSCR) is a well-known congenital digestive disease that originates due to the developmental disorder of neural crest cells. MiR-206 is kown to have a relationship with digestive malfunctions. Therefore, we investigated whether or not miR-206 was involved in the pathogenesis of HSCR. qRT-PCR and Western blot assays were used to detect the expression levels of miRNA and mRNAs, and proteins in case and control tissue samples and two cell lines (293T and SH-SY5Y). The functions of miR-206 in vitro were measured by transwell assay, CCK8 assay and flow cytometry. Finally, we conducted dual-luciferase reporter assay to verify the connections between miR-206 and the target mRNA SDPR. Down-regulation of miR-206 was found in HSCR case tissue samples compared with controls, which was validated to be connected with the increased level of mRNA and protein of SDPR by qRT-PCR and dual-luciferase reporter assay. Moreover, miR-206 suppressed the cell migration and proliferation and silencing of SDPR could rescue the extent of the suppressing effects by miR-206 inhibitor. The findings suggest that miR-206 may play a significant role in the pathogenesis of HSCR, as well as inhibiting the cell migration and proliferation by targeting SDPR in disease models. 

Retracted: No

PubPeer comments:
 Figure 3C appears to have four sets of overlapping panels.  , 
 #1 Thank you very much for your guidance. In 2016, we have published the corrigendum for this result in Scientific reports. Updated result has been published in Sci Rep. 2016 Jan 6; 6: 17666. doi: 10.1038 srep17666 and were available on Pubmed with the PMID: 26732057 . Thanks again for your careful reading and rigorous academic attitude. ,
Androgen receptor regulates expression of skeletal muscle-specific proteins and muscle cell types
Authors: LeRoy A Hanchett
Meng-Yin Tsai
Kuang-Hsiang Chuang
Chawnshang Chang
Qingquan Xu
Saleh Altuwaijri
Dong Kun Lee
Shuyuan Yeh
Huei-Ju Ting
Hong-Chiang Chang
Zhiming Yang
Journal: Endocrine (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: C2C12 myoblasts; androgen receptor; skeletal muscle development; AR gene transcription; skeletal muscle-specific protein expression
Affiliations: George Whipple Lab for Cancer Research, Department of Pathology, The Cancer Center, University of Rochester Medical Center, Rochester, New York 14642, USA.

Abstract:  C2C12 myoblasts expressing the androgen receptor (AR) were used to analyze the role of androgen-AR signaling pathway in skeletal muscle development. Marked up-regulation of AR expression was observed in differentiated myotubes. A nuclear run-on transcription assay demonstrated that transcription of the AR gene is increased during skeletal muscle cell differentiation. Regulation of skeletal muscle-specific protein expression by the androgen-AR signaling pathway was further analyzed using quadriceps skeletal muscle from wild-type (WT) and AR knock-out (ARKO) male mice. A histological analysis of quadriceps skeletal muscle indicates no morphological differences between ARKO and WT mice. However, the androgen-AR signaling pathway increases expression of slow-twitch-specific skeletal muscle proteins and downregulates fast-twitch-specific skeletal muscle proteins, resulting in an increase of slow-twitch muscle fiber type cells in quadriceps muscle. 

Retracted: No

PubPeer comments:
 Figure 2. * Blue boxes: The WT and ARKO H E staining panels appear to show an overlap. Could the authors please check? This figure is important for the conclusion that (from the legend):  No morphological difference in quadriceps muscle from the WT and ARKO mice. . It is also a key factor for a statement in the Abstract:  A histological analysis of quadriceps skeletal muscle indicates no morphological differences between ARKO and WT mice.  ,
Anti-oxidative and Anti-apoptotic Effects of Acupuncture: Role of Thioredoxin-1 in the Hippocampus of Vascular Dementia Rats
Authors: Xue-Rui Wang
Si-Qi Du
Cun-Zhi Liu
Lu-Lu Lin
Chao-Qun Yan
Wen Zhu
Guang-Xia Shi
Na-Na Yang
Journal: Neuroscience (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: acupuncture; apoptosis; oxidative stress; thioredoxin; vascular dementia.
Affiliations: Department of Acupuncture and Moxibustion, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing, China., Department of Acupuncture and Moxibustion, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China., Shandong University of Traditional Chinese Medicine, Jinan, China., Department of Acupuncture and Moxibustion, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address: .

Abstract:  Emerging evidence suggests that acupuncture treatment has anti-oxidative effects that affect cognitive impairment in vascular dementia (VD) rats. In the present study, we aimed to investigate whether thioredoxin-1 (Trx-1)/thioredoxin reductase-1 (TrxR-1) was involved in the beneficial effects of acupuncture. After 2-weeks of acupuncture treatment, Morris water maze (MWM), dihydroethidium (DHE) staining, Nissl staining and TdT-mediated dUTP nick end labeling (TUNEL) staining were used to assess the effects of acupuncture on cognitive function and hippocampal neuronal injury in two-vessel occlusion (2VO) model. The protein and mRNA levels of Trx-1 and TrxR-1, the activity of TrxR-1 as well as the phosphorylation of the apoptosis signal-regulating kinase 1 (ASK1)-c-Jun N-terminal kinase (JNK)/p38 pathway were measured by Western blot, real-time PCR analysis, TrxR-1 activity analysis and immunofluorescence (IF) staining respectively. We found that there were oxidative and apoptotic injury in the CA1 area, accompanied with the decreased expressions of Trx-1 and TrxR-1 in the hippocampus. Acupuncture ameliorated cognitive deficits caused by cerebral ischemic injury and inhibited oxidative stress and neuronal apoptotic injury in the hippocampus. Acupuncture also up-regulated the expressions of Trx-1 and TrxR-1, increased the activity of TrxR-1, accompanied with inhibiting the activation of the ASK1-JNK/p38 pathway. However, the effects of acupuncture on improving cognitive function, inhibiting oxidative stress and neuron apoptotic damage were blocked by Trx-1siRNA. In conclusion, these findings indicated that acupuncture treatment improved VD though anti-oxidative and anti-apoptotic mechanisms which involved the up-regulations of Trx-1/TrxR-1 and inhibitions of ASK1-JNK/p38 pathway. 

Retracted: No

PubPeer comments:
 Figure 2A * Aqua boxes: The  Sham and  2VO+Acu panels appear to look very similar  , 
 Figure 6A. * Green boxes: The 2VO panel appears to show an overlap with the 2VO+trx-1siRNA + Acu panel.  ,
Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling
Authors: Kathryn Davis
Christin Schaaf
River Gunville
Craig H Selzman
Marcio Buffolo
Karla Maria Pires
Roberta A Gottlieb
Natalia S Torres
Sihem Boudina
Journal: Antioxidants & Redox Signaling (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: IGF-1 receptors; autophagy; cardiomyocytes; contractile function; hyperinsulinemia
Affiliations: 1 Department of Nutrition and Integrative Physiology, Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah., 2 Nora Eccles Harrison Cardiovascular Research and Training Institute, Salt Lake City, Utah., 3 Division of Cardiothoracic Surgery, University of Utah School of Medicine, Salt Lake City, Utah., 4 The Smidt Heart Institute, Cedars-Sinai Heart Institute, Los Angeles, California.

Abstract:  Aims: Autophagy is a catabolic process required for the maintenance of cardiac health. Insulin and insulin-like growth factor 1 (IGF-1) are potent inhibitors of autophagy and as such, one would predict that autophagy will be increased in the insulin-resistant/diabetic heart. However, autophagy is rather decreased in the hearts of diabetic/insulin-resistant mice. The aim of this study is to determine the contribution of IGF-1 receptor signaling to autophagy suppression in insulin receptor (IR)-deficient hearts. Results: Absence of IRs in the heart was associated with reduced autophagic flux, and further inhibition of autophagosome clearance reduced survival, impaired contractile function, and enhanced myocyte loss. Contrary to the in vivo setting, isolated cardiomyocytes from IR-deficient hearts exhibited unrestrained autophagy in the absence of insulin, whereas addition of insulin was able to suppress autophagy. To investigate the mechanisms involved in the maintenance of the responsiveness to insulin in IR-deficient hearts, we generated mice lacking both IRs and one copy of the IGF-1 receptor (IGF-1R) in cardiac cells and showed that these mice had increased autophagy. Innovation and Conclusion: This study unveils a new mechanism by which IR-deficient hearts can still respond to insulin to suppress autophagy, in part, through activation of IGF-1R signaling. This is a highly significant observation because it is the first to show that systemic hyperinsulinemia can suppress autophagy in IR-deficient hearts through IGF-1R signaling. 

Retracted: No

PubPeer comments:
  , 
 Original and updated figure are same in correction. https: www.liebertpub.com doi 10.1089 ars.2018.7640.correx?url_ver=Z39.88-2003 rfr_id=ori%3Arid%3Acrossref.org rfr_dat=cr_pub++0pubmed What does  self report mean? Correction made only after comment on PubPeer. https: pubpeer.com publications D811FAFEBF1C71C95CADEC79513691 ,
The putative tumour suppressor microRNA-124 modulates hepatocellular carcinoma cell aggressiveness by repressing ROCK2 and EZH2
Authors: Shu-Peng Chen
Fang Zheng
Xiu-Wu Bian
Marie C Lin
Hsiang-Fu Kung
Yi-Ji Liao
Xin-Yuan Guan
Mu-Yan Cai
Yi-Xin Zeng
Yan-Hui Liu
Tian-Hao Liu
Dan Xie
Journal: Gut (2012)
Discipline: CLINICAL MEDICINE
Keywords: miR-124; hepatocellular carcinoma; expression levels; metastasis; invasion
Affiliations: The State Key Laboratory of Oncology in South China, Sun Yat-Sen University, Guangzhou, China.

Abstract:  Background: Recent profile studies of microRNA (miRNA) expression have documented a deregulation of miRNA (miR-124) in hepatocellular carcinoma (HCC). Objective: To determine the status of miR-124 expression and its underlying mechanisms in the pathogenesis of HCC. Methods: The expression levels of miR-124 were first examined in HCC cell lines and tumour tissues by real-time PCR. The in vitro and in vivo functional effect of miR-124 was examined further. A luciferase reporter assay was conducted to confirm target associations. Results: The expression levels of miR-124 were frequently reduced in HCC cells and tissues, and low-level expression of miR-124 was significantly associated with a more aggressive and/or poor prognostic phenotype of patients with HCC (p&lt;0.05). In HCC cell lines, stable overexpression of miR-124 was sufficient to inhibit cell motility and invasion in vitro, and suppress intrahepatic and pulmonary metastasis in vivo. In addition, ectopic overexpression of miR-124 in HCC cells inhibited epithelial-mesenchymal cell transition, formation of stress fibres, filopodia and lamellipodia. Further studies showed that miR-124 could directly target the 3'-untranslated region (3'-UTR) of both ROCK2 and EZH2 mRNAs, and suppress their mRNA and protein expressions. These findings suggest that miR-124 plays a critical role in regulating cytoskeletal events and epithelial-mesenchymal cell transition and, ultimately, inhibits the invasive and/or metastatic potential of HCC, probably by its direct target on ROCK2 and EZH2 genes. These results provide functional and mechanistic links between the tumour suppressor miRNA-124 and the two oncogenes ROCK2 and EZH2 on the aggressive nature of HCC. Conclusion: These data highlight an important role for miR-124 in the regulation of invasion and metastasis in the molecular aetiology of HCC, and suggest a potential application of miR-124 in prognosis prediction and cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 4A contains two images which appear to overlap.  ,
Low cholesterol triggers membrane microdomain-dependent CD44 shedding and suppresses tumor cell migration
Authors: Hidetoshi Nishiyama
Mitsuo Suga
Kazuhiro Mio
Chikara Sato
Yuusuke Maruyama
Toshiyuki Murai
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CD44; proteolytic cleavage; cholesterol depletion; lipid rafts; ADAM10
Affiliations: Department of Immunology and Microbiology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan. 

Abstract:  CD44 is a cell surface adhesion molecule for hyaluronan and is implicated in tumor invasion and metastasis. Proteolytic cleavage of CD44 plays a critical role in the migration of tumor cells and is regulated by factors present in the tumor microenvironment, such as hyaluronan oligosaccharides and epidermal growth factor. However, molecular mechanisms underlying the proteolytic cleavage on membranes remain poorly understood. In this study, we demonstrated that cholesterol depletion with methyl-Œ≤-cyclodextrin, which disintegrates membrane lipid rafts, enhances CD44 shedding mediated by a disintegrin and metalloproteinase 10 (ADAM10) and that cholesterol depletion disorders CD44 localization to the lipid raft. We also evaluated the effect of long term cholesterol reduction using a statin agent and demonstrated that statin enhances CD44 shedding and suppresses tumor cell migration on a hyaluronan-coated substrate. Our results indicate that membrane lipid organization regulates CD44 shedding and propose a possible molecular mechanism by which cholesterol reduction might be effective for preventing and treating the progression of malignant tumors. 

Retracted: No

PubPeer comments:
  ,
The DNA damage mark pH2AX differentiates the cytotoxic effects of small molecule HDAC inhibitors in ovarian cancer cells
Authors: Florence Wagner
Stephen J Haggarty
Edward Holson
Dineo Khabele
Scott W Hiebert
Daniel M Fass
Srividya Bhaskara
Andrew J Wilson
Yan-Ling Zhang
Stuart L Schreiber
Journal: Cancer biology & therapy (2011)
Discipline: CLINICAL MEDICINE
Keywords: DNA damage response pathways; ovarian cancer; gamma-H2AX phosphorylation; histone deacetylase inhibitors; cell viability
Affiliations: Vanderbilt University School of Medicine, Nashville, TN, USA.

Abstract:  High grade epithelial ovarian cancers are relatively sensitive to DNA damaging platinum-based chemotherapy, suggesting that the dependencies of ovarian tumors on DNA damage response pathways can be harnessed for therapeutic purposes. Our goal was to determine if the DNA damage mark gamma-H2AX phosphorylation (pH2AX) could be used to identify suitable cytotoxic histone deacetylase inhibitors (HDACi) for ovarian cancer treatment. Nineteen chemically diverse HDACi compounds were tested in 7 ovarian cancer cell lines. Fluorescent, biochemical and cell-based assays were performed to assess DNA damage by induction of pH2AX and to measure cell viability and apoptosis. The relationships between pH2AX and the cellular effects of cell viability and apoptosis were calculated. Selected HDACi were tested in combination with cisplatin and other DNA damaging agents to determine if the HDACi improved upon the effects of the DNA damaging agents. The HDACi compounds induced differing levels of pH2AX expression. High levels of pH2AX in HDACi-treated ovarian cancer cells were tightly associated with decreased cell viability and increased apoptosis. Consequently, a ketone-based HDACi was chosen and found to enhance the effects of cisplatin, even in ovarian cancer cells with extreme resistance to DNA damaging drugs. In conclusion, a fluorescent-based assay for pH2AX can be used to determine cellular responses to HDACi in vitro and may be a useful tool to identify potentially more effective HDACi for the treatment of ovarian cancer. In addition, these results lend support to the inclusion of ketone-derived HDACi compounds for future development. 

Retracted: No

PubPeer comments:
 Figure 3: Actin and Tubulin bands are much more similar than expected.  ,
Transforming Growth Factor Beta (TFG-Œ≤) Concentration Isoforms are Diminished in Acute Coronary Syndrome
Authors: Jorge Ram√≥n Padilla-Guti√©rrez
Emmanuel Vald√©s-Alvarado
Juan Arellano-Martin
Jos√© Francisco Mu√±oz Valle
H√©ctor Enrique Flores-Salinas
Sara√≠ Citlalic Rodr√≠guez-Reyes
Yeminia Valle
Journal: Cell biochemistry and biophysics (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Acute coronary syndrome; Cardiac diseases; Protein isoforms; Serum concentration; TGF-Œ≤ concentration.
Affiliations: Instituto de Investigaci√≥n en Ciencias Biom√©dicas, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico., Doctorado en Ciencias Biom√©dicas, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico., Especialidad en Cardiolog√≠a IMSS, Centro Universitario de Ciencias de la Salud, Guadalajara, Jalisco, Mexico., Unidad M√©dica de Alta Especialidad, Centro M√©dico Nacional de Occidente, Departamento de Cardiolog√≠a, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Mexico., Instituto de Investigaci√≥n en Ciencias Biom√©dicas, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico. .

Abstract:  Acute coronary syndrome (ACS) is the leading cause of death in elderly patients worldwide. Due its participation in apoptosis, fibrosis, and angiogenesis, transforming growth factor-Œ≤ (TGF-Œ≤) isoforms had been categorized as risk factors for cardiovascular diseases. However, due their contradictory activities, a cardioprotective role has been suggested. The aim was to measure the plasma levels of TGF-Œ≤1, 2, and 3 proteins in patients with ACS. This was a case-control study including 225 subjects. The three activated isoforms were measured in serum using the Bio-Plex Pro TGF-Œ≤ assay by means of magnetic beads; the fluorescence intensity of reporter signal was read in a Bio-Plex Magpix instrument. We observed a significant reduction of the three activated isoforms of TGF-Œ≤ in patients with ACS. The three TGF-Œ≤ isoforms were positively correlated with each other in moderate-to-strong manner. TGFŒ≤-2 was inversely correlated with glucose and low-density lipoprotein (LDL)-cholesterol, whereas TGF-Œ≤3 was inversely correlated with the serum cholesterol concentration. The production of TGF-Œ≤1, TGF-Œ≤2, and TGF-Œ≤3 are decreased in the serum of patients with ACS. Further follow-up controlled studies with a larger sample size are needed, in order to test whether TGF-Œ≤ isoforms could be useful as biomarkers that complement the diagnosis of ACS. 

Retracted: No

PubPeer comments:
 The title and the line#6 on page 437 should read TGF instead of TFG. A small typo but TFG is another protein. ,
The softness of tumour-cell-derived microparticles regulates their drug-delivery efficiency
Authors: Zhaohan Wei
Xiaolong Shi
Haiyan Zhao
Tuying Yong
Ke Tang
Xiangliang Yang
Nana Bie
Qingle Liang
Bo Huang
Lu Gan
Xiaoqiong Zhang
Haibo Jia
Wei Huang
Journal: Nature Biomedical Engineering (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Extracellular microparticles; drug-delivery; tumour-repopulating cells; softness; three-dimensional fibrin gels
Affiliations: National Engineering Research Center for Nanomedicine, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China., Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China., Institute of Computing Science and Technology, Guangzhou University, Guangzhou, China., School of Artificial Intelligent and Automation, Huazhong University of Science and Technology, Wuhan, China., Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China., National Engineering Research Center for Nanomedicine, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China. ., Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica, Huazhong University of Science and Technology, Wuhan, China. ., Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. ., Department of Immunology and National Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. .

Abstract:  Extracellular microparticles (MPs) can function as drug-delivery vehicles for anticancer drugs. Here, we show that the softness of MPs derived from tumour-repopulating cells (TRCs) isolated from three-dimensional fibrin gels enhances the MPs' drug-delivery efficiency. We found that, compared with MPs derived from tumour cells cultured in conventional tissue-culture plastic, TRC-derived MPs intravenously injected in tumour-xenograft-bearing mice showed enhanced accumulation in tumour tissues, enhanced blood-vessel crossing and penetration into tumour parenchyma, and preferential uptake by highly tumorigenic TRCs. We also show that the cytoskeleton-related protein cytospin-A plays a critical role in the regulation of TRC-derived MP softness. The modulation of the mechanical properties of TRC-derived MPs could aid the efficiency of delivery of anticancer drugs. 

Retracted: No

PubPeer comments:
 A micrograph has been duplicated and presented as something else in Figure S23a. Question regarding the TEM data presented in Figure 1: How did you prepare the samples and which fixation and contrast enhancement did you use? Question regarding the confocal microscopy data presented in Figure 1: The main images are of lower resolution (more pixelated) compared to the zoomed in images, and they don t seem to correspond to each other. Why?   ,
Vitamin C supplementation reduces the odds of developing a common cold in Republic of Korea Army recruits: randomised controlled trial
Authors: H R Lim
Tae Kyung Kim
J S Byun
Journal: BMJ Military Health (2020)
Discipline: CLINICAL MEDICINE
Keywords: URI; common cold; high doses; military personnel; vitamin c.
Affiliations: Department of Public Health, Yonsei University, Seoul, South Korea ., Department of Health policy & Management, Armed Forces Medical Command, Seongnam, South Korea., Department of Clinical Medicine, Armed Forces Medical School, Daejeon, South Korea., Department of Inspection, Armed Forces Medical Command, Seongnam, South Korea.

Abstract:  Introduction: The Republic of Korea (ROK) military has a high incidence of respiratory diseases at training centres. Vitamin C has been reported to reduce the incidence of colds. For the purpose of preventing soldiers' respiratory diseases, this study aimed to investigate whether vitamin C intake can prevent common colds in the ROK Army soldiers. Methods: This was a randomised, placebo-controlled, and double-blind trial of soldiers who enlisted in the Korea Army Training Centre for 30 days from 12 February to 13 March 2018. The study participants were divided into groups (vitamin C vs placebo). The military medical records were searched to determine whether the participants had a common cold. Multiple logistic regression analysis was performed to identify the association between vitamin C intake and diagnosis of common colds. In addition, subgroup analysis on the relationship between vitamin C intake and common cold according to smoking status, training camp and physical rank was conducted. Results: A total of 1444 participants were included in our study. Of these participants, 695 received vitamin C (6000 mg/day, vitamin C group), while 749 participants received placebo (0 mg/day, placebo group). The vitamin C group had a 0.80-fold lower risk of getting a common cold than did the placebo group. Subgroup analyses showed that this effect was stronger among subjects in camp A, among never smokers and among those in physical rank 3. Conclusion: Vitamin C intake provides evidence to suggest that reducing the common colds in Korean Army soldiers. Our results may serve as a basis for introducing military healthcare policies that can provide vitamin C supplementation for military personnel in basic military training. 

Retracted: No

PubPeer comments:
 See description of statistical problems in the trial at: https: militaryhealth.bmj.com content early 2020 03 05 bmjmilitary-2019-001384.responses ,
Correlation between endometrial receptivity with expressions of IL-1 and VEGF in rats with polycystic ovary syndrome
Authors: Y-H Shan
Q-L Qu
L Jiang
D-M Zhao
F-H Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: endometrial receptivity; interleukin-1; vascular endothelial growth factor; PCOS; rats
Affiliations: Department of Reproductive Medicine, Yantai Yuhuangding Hospital, Yantai, China. .

Abstract:  Objective: To investigate the correlation between endometrial receptivity with expressions of interleukin-1 (IL-1) and vascular endothelial growth factor (VEGF) in rats with polycystic ovary syndrome (PCOS). Materials and methods: A total of 24 female Sprague-Dawley (SD) 21 days old were randomly divided into control group (n=12) and PCOS group (n=12). Rats in the control group were normally raised, and PCOS model was established in rats of the PCOS group. All the rats were sacrificed when they grew to 80 days old. Immunohistochemistry was applied to detect the expressions of IL-1 and VEGF. Western blotting was performed to measure the relative expressions of IL-1 and VEGF proteins. Quantitative Polymerase Chain Reaction (qPCR) was utilized to determine the relative messenger ribonucleic acid (mRNA) expressions of IL-1 and VEGF. Data related to endometrial receptivity were detected. Results: The expression levels of IL-1 and VEGF in the PCOS group declined markedly compared with those in the control group, and the differences were statistically significant (p&lt;0.05). PCOS group had notably lower protein expressions of IL-1 and VEGF than the control group, with statistically significant differences (p&lt;0.05). The mRNA expressions of IL-1 and VEGF in PCOS group were significantly lower than those in the control group, displaying statistically significant differences (p&lt;0.05). Compared with that in the control group, the endometrial receptivity of rats in the PCOS group was reduced evidently, and the difference was statistically significant (p&lt;0.05). Both IL-1 and VEGF had positive correlations with the endometrial receptivity. Conclusions: Both IL-1 and VEGF are positively correlated with the endometrial receptivity in the case of PCOS, which can serve as therapeutic targets for PCOS and improve endometrial receptivity in the future. 

Retracted: No

PubPeer comments:
 The Western blots in this paper show resemblance to those in other papers from different research groups. Here is Figure 2 from this paper:  Compare to : * Figure 3 from XM Sun et al (2019): https: pubpeer.com publications 9319E643F702A1E9267F76FBDF0866 * Figure 3 from Y Long et al (2019): https: pubpeer.com publications 94DBAB3CDCF9D7C00792762576D297 * Figure 4 from HD Lou et al (2019): https: pubpeer.com publications D1194F22B8521E1BBF96F17D378181 * Figure 5 from XD Pan et al (2019): https: pubpeer.com publications A8530707339CB1A5287E7FFBD46CFE  or to:  Both taken from compositions by Hoya Camphorifolia. , 
 Fig 4.  A, Correlation between protein expression of IL-1 and thickness of the endometrium. B, Correlation between protein expression of VEGF and thickness of the endometrium.  ,
Enhanced electrocatalytic activity and durability of highly monodisperse Pt@PPy‚ÄìPANI nanocomposites as a novel catalyst for the electro-oxidation of methanol
Authors: √ñzlem Karatepe
Yunus Yƒ±ldƒ±z
Handan Pamuk
Sinan Eris
Zeynep Dasdelen
Fatih Sen
Journal: RSC Advances (2016)
Discipline: CHEMISTRY
Keywords: Pt nanocomposites; PPy; PANI; DMAB; XRD
Affiliations: Sen Research Group, Biochemistry Department, Faculty of Arts and Science, Dumlupƒ±nar University, 43100 K√ºtahya

Abstract: Highly monodisperse Pt nanocomposites (Pt@PPy‚ÄìPANI NPs) supported on polypyrrole (PPy)‚Äìpolyaniline (PANI) have been successfully synthesized for the first time by a simple one-pot process, which involves the simultaneous reduction of the conducting polypyrrole (PPy)‚Äìpolyaniline (PANI) and Pt precursors using DMAB (dimethylamine borane) as a reductant under ultrasonic conditions. Pt@PPy‚ÄìPANI NPs have been characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM), and X-ray photoelectron spectroscopy (XPS). All the results show that highly crystalline and stable colloidal Pt@PPy‚ÄìPANI NPs have been formed as one of the most active and long-lived catalysts with superior reusability performance for the electro-oxidation of methanol at room temperature. Compared to PPy or PANI supported Pt nanoparticles, Pt@PPy‚ÄìPANI NPs exhibit extraordinary electrocatalytic activity and stability toward the electro-oxidation of methanol, showing their potential use as a new electrode material for direct methanol fuel cells (DMFCs). It should be primarily attributed to the PPy‚ÄìPANI, which not only provided larger surface area and flaws for the deposition of Pt nanoparticles, but also the adsorption of more methanol molecules for further oxidation.

Retracted: Yes

PubPeer comments:
null, 
 No comment is provided by the complainant , 
 No comment is provided by the complainant , 
 Compare images inside the same coloured rectangles, and compare images underlined by the same coloured lines. ,
Exosomal long non-coding RNA GAS5 suppresses Th1 differentiation and promotes Th2 differentiation via downregulating EZH2 and T-bet in allergic rhinitis
Authors: Xueping Wang
Xiaoyuan Zhu
Yulin Zhao
Ying Wang
Journal: Molecular Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: EZH2; Exosome; GAS5; Helper T cell differentiation; T-bet.
Affiliations: Department of Rhinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. Electronic address: .

Abstract:  The imbalance of helper T cell (Th) 1/Th2 differentiation is involved in the development of allergic rhinitis (AR). Recent studies reveal the regulatory function of exosomes on Th1/Th2 differentiation. However, the key mediator in exosomes that modulate such response remains unclear. In this study, the expression of long-noncoding RNA GAS5 (LncGAS5) was detected in exosomes which were isolated from AR patient nasal mucus (AR-EXO) and ovalbumin (OVA)-stimulated nasal epithelial cells (OVA-EXO). Th1/Th2 differentiation was induced in na√Øve CD4+ T cells, and the percentage of IFN-Œ≥ expressing cells (Th1 cells) and IL-4 expressing cells (Th2 cells) was detected using flow cytometry. The result showed that LncGAS5 was upregulated in AR epithelial samples, AR-EXO, and OVA-EXO. The coincubation of AR-EXO and CD4+ T cells suppressed Th1 differentiation and promoted Th2 differentiation, which is mediated by LncGAS5 in AR-EXO. The LncGAS5 in AR-EXO inhibited transcription and expression of EZH2, and it also inhibited T-bet expression at mRNA and protein levels. The gain-of-function and loss-of-function experiments suggested that LncGAS5 mediates Th1/Th2 differentiation partly through downregulating T-bet and EZH2. In summary, our findings demonstrated that LncGAS5 in AR epithelium-derived exosomes is the key mediator in Th1/Th2 differentiation, providing a possible therapeutic target of AR. 

Retracted: No

PubPeer comments:
 In Figure 1B and D, a micrograph has been duplicated and presented as something else. The anti-CD63 Western immunoblot lacks the usual smearing and I doubt that it s CD63. Furthermore, all the Western immunoblots show diffuse bands, similar to the artificial blots presented by the many papermill producers from China.  ,
Microscopic enteritis: Bucharest consensus
Authors: Matt W Johnson
Mihai Danciu
A Salvador Pe√±a
Umberto Volta
Gabrio Bassotti
Mohammad Rostami-Nejad
Sauid Ishaq
Amitabh Srivastava
Marie Robert
Vincenzo Villanacci
Mohammad H Derakhshan
Geoffrey Holmes
David S Sanders
Kamran Rostami
David Aldulaimi
Kamran Ghafarzadegan
Gabriel Becheanu
Michael N Marsh
Luke Materacki
James J Going
Jean-Fran√ßois Fl√©jou
Carlo Catassi
Journal: World journal of gastroenterology (2015)
Discipline: CLINICAL MEDICINE
Keywords: Bucharest consensus; Enteropathy; Gluten; Malabsorption; Microscopic enteritis
Affiliations: Kamran Rostami, David Aldulaimi, Luke Materacki, Department of Gastroenterology, Alexandra Hospital, Worcestershire B98 7UB, United Kingdom.

Abstract:  Microscopic enteritis (ME) is an inflammatory condition of the small bowel that leads to gastrointestinal symptoms, nutrient and micronutrient deficiency. It is characterised by microscopic or sub-microscopic abnormalities such as microvillus changes and enterocytic alterations in the absence of definite macroscopic changes using standard modern endoscopy. This work recognises a need to characterize disorders with microscopic and submicroscopic features, currently regarded as functional or non-specific entities, to obtain further understanding of their clinical relevance. The consensus working party reviewed statements about the aetiology, diagnosis and symptoms associated with ME and proposes an algorithm for its investigation and treatment. Following the 5(th) International Course in Digestive Pathology in Bucharest in November 2012, an international group of 21 interested pathologists and gastroenterologists formed a working party with a view to formulating a consensus statement on ME. A five-step agreement scale (from strong agreement to strong disagreement) was used to score 21 statements, independently. There was strong agreement on all statements about ME histology (95%-100%). Statements concerning diagnosis achieved 85% to 100% agreement. A statement on the management of ME elicited agreement from the lowest rate (60%) up to 100%. The remaining two categories showed general agreement between experts on clinical presentation (75%-95%) and pathogenesis (80%-90%) of ME. There was strong agreement on the histological definition of ME. Weaker agreement on management indicates a need for further investigations, better definitions and clinical trials to produce quality guidelines for management. This ME consensus is a step toward greater recognition of a significant entity affecting symptomatic patients previously labelled as non-specific or functional enteropathy. 

Retracted: No

PubPeer comments:
  , 
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Mannan-degrading enzymes from Cellulomonas fimi
Authors: R A Warren
D Stoll
H St√•lbrand
Journal: Applied and Environmental Microbiology (1999)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: genes; man26a; man2A; Cellulomonas fimi; mannanase 26A
Affiliations: Department of Microbiology and Immunology and The Protein Engineering Network of Centres of Excellence, The University of British Columbia, Vancouver, British Columbia, Canada.

Abstract:  The genes man26a and man2A from Cellulomonas fimi encode mannanase 26A (Man26A) and beta-mannosidase 2A (Man2A), respectively. Mature Man26A is a secreted, modular protein of 951 amino acids, comprising a catalytic module in family 26 of glycosyl hydrolases, an S-layer homology module, and two modules of unknown function. Exposure of Man26A produced by Escherichia coli to C. fimi protease generates active fragments of the enzyme that correspond to polypeptides with mannanase activity produced by C. fimi during growth on mannans, indicating that it may be the only mannanase produced by the organism. A significant fraction of the Man26A produced by C. fimi remains cell associated. Man2A is an intracellular enzyme comprising a catalytic module in a subfamily of family 2 of the glycosyl hydrolases that at present contains only mammalian beta-mannosidases. 

Retracted: No

PubPeer comments:
 Concern over extensive noise overlap in these two figures (see image here):  ,
Carnosic acid potentiates the anticancer effect of temozolomide by inducing apoptosis and autophagy in glioma
Authors: Rong Wang
Feng Zhi
Qing Lan
Jiahao Mao
Naiyuan Shao
Lian Xue
Journal: Journal of Neuro-Oncology (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Apoptosis; Autophagy; Carnosic acid; Glioma; Temozolomide.
Affiliations: Department of Neurosurgery, Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China., Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, #1055 Sanxiang Road, Suzhou, Jiangsu, China., Modern Medical Research Center, The Third Affiliated Hospital of Soochow University, #185 Juqian Road, Changzhou, Jiangsu, China., Department of Neurosurgery, Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China. ., Modern Medical Research Center, The Third Affiliated Hospital of Soochow University, #185 Juqian Road, Changzhou, Jiangsu, China. ., Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, #1055 Sanxiang Road, Suzhou, Jiangsu, China. .

Abstract:  Objective: Malignant glioma is a lethal brain tumor with a low survival rate and poor prognosis. New strategies are urgently needed to augment the chemotherapeutic effects of temozolomide (TMZ), the standard drug in glioma treatment. Carnosic acid (CA) has been reported to have anticancer, antioxidant and anti-infectious properties. In this study, we aimed to investigate the anticancer effects and the underlying mechanisms of CA in combination with TMZ in glioma cancer cells. Methods: The glioma cancer cells were treated with TMZ, CA, or TMZ + CA. We evaluated cell survival by CCK-8 assay, cell anchorage-independent survival by colony formation assay, cell migration by wound-healing assay, cell cycle and cell apoptosis by flow cytometry, and protein expression by western blot. Results: CA enhanced the cytotoxic effect of TMZ in glioma cancer cells. CA enhanced TMZ-induced inhibition of colony formation and cell migration and enhanced TMZ-induced cell cycle arrest and cellular apoptosis. Immunofluorescence suggested that CA in combination with TMZ triggered autophagy. Furthermore, CA promoted TMZ-induced cell cycle arrest and cellular apoptosis by Cyclin B1 inhibition and activation of PARP and Caspase-3, while CA promoted TMZ-induced cellular autophagy by p-AKT inhibition, p62 downregulation and LC3-I to LC3-II transition. Conclusion: These data suggest that the combination therapy of CA and TMZ strengthens the anticancer effect of TMZ by enhancing apoptosis and autophagy. 

Retracted: No

PubPeer comments:
 Figure 2F was brought to my attention by a reader. * Boxes of the same color highlight panels that look more similar than expected.  , 
 An additional concern observed in Figures 4 and 5. * Pink boxes: the Cyclin B1 panel in Figure 4E looks remarkably similar to the p62 panel in Figure 5I.  ,
Inhibition of hepatitis C virus nonstructural protein, helicase activity, and viral replication by a recombinant human antibody clone
Authors: Robert F Garry
Ramesh Prabhu
Roberto Burioni
Nutan Khalap
Srikanta Dash
Massimo Clementi
Journal: American Journal Of Pathology (2004)
Discipline: CLINICAL MEDICINE
Keywords: Hepatitis C virus; NS3; helicase; antibody; replication
Affiliations: Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, 1430 Tulane Ave., New Orleans LA 70112, USA.

Abstract:  Hepatitis C virus (HCV) nonstructural protein 3 (NS3), with its protease, helicase, and NTPase enzymatic activities, plays a crucial role in viral replication, and therefore represents an ideal target for the development of anti-viral agents. We have developed a recombinant human antibody (Fab) that reacts with the helicase domain of HCV NS3. The affinity-purified Fab antibody completely inhibited the helicase activity of HCV NS3 at equimolar concentration. To evaluate the effect of the Fab on HCV replication, the clone encoding the Fab gene was put into an expression vector, which converts Fab into a complete IgG1 antibody. Using a DNA-based transfection model, we demonstrated that intracellular expression of this antibody resulted in significant reduction of HCV-negative strand RNA synthesis. Intracellular expression of this antibody into either a stable cell line replicating subgenomic RNA, or a transient full-length HCV replication model, reduced both HCV RNA and viral protein expression. These results support the use of recombinant antibody fragments to inhibit NS3 enzyme as a novel, feasible, and effective approach for inhibiting HCV replication. 

Retracted: No

PubPeer comments:
 Figure 10. * Orange boxes: In the top part of the figure, the left panels look very similar. Would that be expected? * Green boxes: In the bottom part of the figure, the left panels look very similar. Would that be expected?  Also, Figure 10 looks remarkably similar to Figure 5 in another paper by the same research group, i.e. Ramesh Prabhu et al., Experimental and Molecular Pathology (2004), DOI: 10.1016 j.yexmp.2004.01.004 https: pubpeer.com publications 0A98892278F5CC4983F7218AF3A057  ,
Circ_0091579 promotes proliferative ability and metastasis of liver cancer cells by regulating microRNA-490-3p
Authors: H Zang
B Zhu
P Zhang
W-Y Niu
L Chen
W-B Shao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Circular RNA 0091579; liver cancer; progression; molecular mechanism; qPCR
Affiliations: Department of Hepatobiliary Surgery, Nantong First People's Hospital, the Second Affiliated Hospital of Nantong University, Nantong, China. .

Abstract:  Objective: To explore the role of Circular RNA 0091579 in the progression of liver cancer (LCa) and its molecular mechanism. Patients and methods: Quantitative polymerase chain reaction (qPCR) was used to detect circ_0091579 expression levels in LCa tissues and adjacent tissues, which was further verified in LCa cells and normal liver epithelial cells. After circ_0091579 was knocked down in Huh7 and HepG2 cells, cell counting kit-8 (CCK-8), plate cloning and transwell assays were performed to verify the effect of circ_0091579 on cell proliferative ability and metastasis of LCa cells. The starBase database was used to search for microRNAs that could interact with circ_0091579, and the Dual-Luciferase reporter gene was used to verify their binding relationship. Results: circ_0091579 was highly expressed in HCC and HCC cells. In vitro experiments showed that down-regulation of circ_0091579 expression could remarkably inhibit the proliferative ability and metastasis of HCC cells. Bioinformatics software predicted the binding sites between circ_0091579 and microRNA-490-3p, and dual-luciferase reporter gene assay confirmed the binding relationship between circ_0091579 and microRNA-490-3p. qPCR results showed that microRNA-490-3p was remarkably down-regulated in LCa tissues. In vitro experiments confirmed that overexpression of microRNA-490-3p inhibited the proliferative ability and metastasis of HCC cells. Conclusions: circ_0091579 is abnormally highly expressed in LCa tissues and cells. Down-regulation of circ_0091579 can inhibit the proliferative ability and metastasis of HCC cells by regulating microRNA-490-3p, thus accelerating the progress of the tumor. 

Retracted: No

PubPeer comments:
 Figure 2D. Some repetitive features, in particular in the HepG2 panels. Boxes of the same color focus attention to the most obvious ones, but there are several smaller ones as well that I left unmarked.  , 
 Fig. 4D https: imgur.com a sx6CxOB ,
An electrochemical sensor modified with poly(3,4-ethylenedioxythiophene)-wrapped multi-walled carbon nanotubes for enzyme inhibition-based determination of organophosphates
Authors: Kaur, Navpreet
Thakur, Himkusha
Kumar, Rajesh
Prabhakar, Nirmal
Journal: Microchimica Acta (2016)
Discipline: CHEMISTRY
Keywords: acetylcholinesterase; organophosphates; nanocomposite; poly(3,4-ethylenedioxythiophene); multi-walled carbon nanotubes

Abstract: We report&nbsp;on an acetylcholinesterase (AChE) based sensor for the determination of organophosphates (OPs). A nanocomposite consisting of poly(3,4-ethylenedioxythiophene) (PEDOT; a conducting polymer) and functionalized multi-walled carbon nanotubes (f-MWCNTs) was used as a host matrix for covalent immobilization of AChE. The unique properties of PEDOT and f-MWCNTs proved to be highly efficient for retaining the activity and stability of AChE. The effects of pH value of the phosphate buffer, concentration of enzyme, substrate concentration and incubation time were optimized using chlorpyrifos-methyl as a model OP as it exerts a strong inhibitory effect on AChE. Differential pulse voltammetry (DPV) analysis performed at +0.15&nbsp;V revealed a linear relation of current in respect to chlorpyrifos-methyl concentration range (0.001 to 50 ppb) with 0.001&nbsp;ppb as a detection limit. The sensor can be regenerated to 97% of its activity by applying 2-pyridine aldoxime methiodide (2-PAM) as a regenerating agent. It can be re-used up to six times and stored up to one month. The sensor was applied to the determination of chlorpyrifos-methyl in spiked lettuce where it gave recoveries ranging between 95 and 97%.

Retracted: No

PubPeer comments:
 Compare with the paper Conducting polymer and multi-walled carbon nanotubes nanocomposites based amperometric biosensor for detection of organophosphate doi: 10.1016 j.jelechem.2016.05.037. The two papers are published in the same period. Feb to Mar of 2016. The data points in both figures are in the same location of the figure, however, the values are totally different.   , 
 Figure 1C in this paper  is similar to Figure 1C in Journal of Electroanalytical Chemistry 775 (2016) 121u2013128, 10.1016 j.jelechem.2016.05.037  with some obvious change in scaling between the 2 images. ,