PReD-Bench/PRed-Bench huggingface dataset:
Study of the adjuvanticity of lysine lipopeptides; carbamate analogs elicit strong Th1 and Th2 response to ovalbumin in mice
Authors: G N Qazi
Syed Shafi
Tabasum Ismail
Tabasum Sidiq
M Sarwar Alam
H M Sampath Kumar
Amit Gupta
Doma Mahendhar Reddy
Anamika Khajuria
Journal: International Immunopharmacology (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Bacterial lipoproteins; immune modulators; adjuvanticity; lipidated dipeptides; tripeptides
Affiliations: Synthetic and Biological Chemistry Division, Indian Institute of Integrative Medicine, Jammu 180001, India.

Abstract:  Bacterial lipoproteins and their synthetic analogs are strong immune modulators of the early host responses. In view of the strong adjuvanticity of bacterial lipopeptide mimics bearing lysine residues, a focused library of lipidated dipeptides and tripeptides has been synthesized with a view to understand the pattern of activity vis a vis the site and extent of lipidation. Compounds 4, 5 and 14 stimulate OVA specific IgG titer, neutralization of antibodies (IgG1 and IgG2a), T lymphocyte sub-sets (CD4/CD8) and its production of soluble mediators for Th1 (IFN-γ)/Th2 (IL-4) cytokines and costimulatory molecules (CD80/CD86) which are ideal traits of immune adjuvants. The results support lipidated lysine dipeptides as potent enhancers of humoral and cell mediated immune responses and thus might become promising immune-adjuvants for self adjuvanted vaccines. 

Retracted: No

PubPeer comments:
 Indicated panels are more similar than one would expect. ![file] , 
 Fig 5 panels: These three panels look remarkably similar to each other. Would authors explain how? ![file] ,
Bufalin Inhibits HCT116 Colon Cancer Cells and Its Orthotopic Xenograft Tumor in Mice Model through Genes Related to Apoptotic and PTEN/AKT Pathways
Authors: Jie Wang
Qinsong Zuo
Zhongxiang Gao
Ronghua Zhao
Jie Xu
Chao Chen
Peihao Yin
Teng Chen
Dianxu Feng
Yong Zhang
Shiying Wang
Journal: Gastroenterology Research and Practice (2015)
Discipline: CLINICAL MEDICINE
Keywords: Bufalin; colorectal cancer; cell proliferation; apoptosis; cycle arrest
Affiliations: Department Surgery, Putuo Hospital, University of Traditional Chinese Medicine in Shanghai, Shanghai 200062, China.

Abstract:  Aims. To investigate the anticolorectal cancer (CRC) effects of Bufalin, a bioactive polyhydroxysteroid from Venenum Bufonis, using HCT116 human CRC cell and an established orthotopic xenograft model in mice, and to explore the mechanisms of action. Material and Methods. Cultured HCT116 cells or BALB/c mice with orthotopic tumor were treated by Bufalin (positive control: 5-FU). Cell proliferation, apoptosis, and cycling were determined by MTT, Annexin V/PI staining, and flow cytometry, respectively. In mice, tumor inhibition rate and animal survival were calculated. The expressions of PTEN/phosphate-PTEN, AKT/phosphate-AKT, Bad, Bcl-xl, Bax, or Caspase-3 in cells and/or tumors were determined by Western blot or immunohistochemical staining. Results. Bufalin significantly inhibited cell proliferation and induced cell apoptosis and cycle arrest in a dose/time-dependent manner. In the animal model, Bufalin treatment resulted in significant inhibition of tumor growth and prolonged survival. In the Bufalin-treated cultured cells and/or xenograft tumors, the expressions of PTEN, Bad, Bax, and Caspase-3 were significantly increased, while p-AKT and Bcl-xL significantly decreased. Conclusions. Our results indicate that Bufalin inhibit cell proliferation and orthotopic tumor growth by inducing cell apoptosis through the intrinsic apoptotic pathway, which is of pivotal significance in the identification of an anticancer drug that may synergize with Bufalin. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have two images which overlap. *** ![file] ,
Graft IL-33 regulates infiltrating macrophages to protect against chronic rejection
Authors: Lisa R Mathews
Jenna L Dziki
Simon C Watkins
Tengfang Li
Anna S Roessing
Sruti Shiva
George S Hussey
Steven A Webber
Quan Liu
Martin H Oberbarnscheidt
Michelle Wood-Trageser
Murugesan Velayutham
Joe G Bartolacci
James D Wilkinson
Helong Dai
Yoojin C Lee
Steven J Mullet
Anthony J Demetris
Stacy G Wendell
Zhongqiang Zhang
Hēth R Turnquist
Gaelen K Dwyer
Stephen F Badylak
Journal: Journal of Clinical Investigation (2020)
Discipline: CLINICAL MEDICINE
Keywords: Immunology; Immunotherapy; Macrophages; Organ transplantation; Transplantation.
Affiliations: Department of Surgery and., McGowan Institute for Regenerative Medicine and., Pittsburgh Heart, Lung, and Blood, Vascular Medicine Institute and., Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA., Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Department of Pediatrics, Vanderbilt School of Medicine, Nashville, Tennessee, USA., Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Abstract:  Alarmins, sequestered self-molecules containing damage-associated molecular patterns, are released during tissue injury to drive innate immune cell proinflammatory responses. Whether endogenous negative regulators controlling early immune responses are also released at the site of injury is poorly understood. Herein, we establish that the stromal cell-derived alarmin interleukin 33 (IL-33) is a local factor that directly restricts the proinflammatory capacity of graft-infiltrating macrophages early after transplantation. By assessing heart transplant recipient samples and using a mouse heart transplant model, we establish that IL-33 is upregulated in allografts to limit chronic rejection. Mouse cardiac transplants lacking IL-33 displayed dramatically accelerated vascular occlusion and subsequent fibrosis, which was not due to altered systemic immune responses. Instead, a lack of graft IL-33 caused local augmentation of proinflammatory iNOS+ macrophages that accelerated graft loss. IL-33 facilitated a metabolic program in macrophages associated with reparative and regulatory functions, and local delivery of IL-33 prevented the chronic rejection of IL-33-deficient cardiac transplants. Therefore, IL-33 represents what we believe is a novel regulatory alarmin in transplantation that limits chronic rejection by restraining the local activation of proinflammatory macrophages. The local delivery of IL-33 in extracellular matrix-based materials may be a promising biologic for chronic rejection prophylaxis. 

Retracted: No

PubPeer comments:
 In FIG 1 POD3 and POD94 may have been mixed up according to the supplemental FIG 1. ![file] ,
Atorvastatin overcomes gefitinib resistance in KRAS mutant human non-small cell lung carcinoma cells
Authors: D Liu
H Shi
J Yuan
B Liu
X Zhang
H Bi
J Chen
J Hou
J Liu
L Yue
C Zhang
X Wen
Journal: Cell death & disease (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: statins; gefitinib resistance; non-small cell lung cancer; KRAS mutation; PIK3CA
Affiliations: State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100191, China.

Abstract:  The exact influence of statins on gefitinib resistance in human non-small cell lung cancer (NSCLC) cells with KRAS mutation alone or KRAS/PIK3CA and KRAS/PTEN comutations remains unclear. This work found that transfection of mutant KRAS plasmids significantly suppressed the gefitinib cytotoxicity in Calu3 cells (wild-type KRAS). Gefitinib disrupted the Kras/PI3K and Kras/Raf complexes in Calu3 cells, whereas not in Calu3 KRAS mutant cells. These trends were corresponding to the expression of pAKT and pERK in gefitinib treatment. Atorvastatin (1 μM) plus gefitinib treatment inhibited proliferation, promoted cell apoptosis, and reduced the AKT activity in KRAS mutant NSCLC cells compared with gefitinib alone. Atorvastatin (5 μM) further enhanced the gefitinib cytotoxicity through concomitant inhibition of AKT and ERK activity. Atorvastatin could interrupt Kras/PI3K and Kras/Raf complexes, leading to suppression of AKT and ERK activity. Similar results were also obtained in comutant KRAS/PTEN or KRAS/PIK3CA NSCLC cells. Furthermore, mevalonate administration reversed the effects of atorvastatin on the Kras/Raf and Kras/PI3K complexes, as well as AKT and ERK activity in both A549 and Calu1 cells. The in vivo results were similar to those obtained in vitro. Therefore, mutant KRAS-mediated gefitinib insensitivity is mainly derived from failure to disrupt the Kras/Raf and Kras/PI3K complexes in KRAS mutant NSCLC cells. Atorvastatin overcomes gefitinib resistance in KRAS mutant NSCLC cells irrespective of PIK3CA and PTEN statuses through inhibition of HMG-CoA reductase-dependent disruption of the Kras/Raf and Kras/PI3K complexes. 

Retracted: No

PubPeer comments:
 Figure 1 shows two different strains (rows) and two different antibodies (columns). However, panels A, B, and C appear to show areas of overlap, as highlighted with blue and magenta boxes. Could the authors please check? ![file] , 
 July 2020 Erratum: https: www.ajtmh.org view journals tpmd 103 2 article-p928.xml It reads:  *The authors of an article previously published by the AJTMH (Monoclonal Antibodies for the Diagnosis of Borrelia crocidurae by Fotso Fotso and others draw attention to errors in Figure 1 of that article. These resulted from errors by a researcher that were missed by other authors. Specifically, a single image was inappropriately inserted to represent three different experiments. A corrected Figure 1 is shown below.* Could the authors please clarify how  a single image was inappropriately inserted to represent three different experiments ? Was this caused by inappropriately labeling of experimental results? ,
Mitochondrial dysfunction induces formation of lipid droplets as a generalized response to stress
Authors: Seon-Jin Lee
Jinglan Zhang
Hong Pyo Kim
Augustine M K Choi
Journal: Oxidative Medicine and Cellular Longevity (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Lipid droplet formation; cellular stress; metabolism; oxidative phosphorylation; glycolysis
Affiliations: Biomedical Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 305-806, Republic of Korea., Department of Surgical Intensive Care Unit, Capital Medical University Affiliated Beijing Anzhen Hospital, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing 100029, China, Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA, School of Pharmacy, Ajou University, Suwon 443-749, Republic of Korea

Abstract:  Lipid droplet (LD) formation is a hallmark of cellular stress. Cells attempt to combat noxious stimuli by switching their metabolism from oxidative phosphorylation to glycolysis, sparing resources in LDs for generating cellular reducing power and for anabolic biosynthesis. Membrane phospholipids are also a source of LDs. To elucidate the formation of LDs, we exposed mice to hyperoxia, hypoxia, myocardial ischemia, and sepsis induced by cecal ligation and puncture (CLP). All the above-mentioned stressors enhanced the formation of LDs, as assessed by transmission electron microscopy, with severe mitochondrial swelling. Disruption of mitochondria by depleting mitochondrial DNA ( ρ 0 cells) significantly augmented the formation of LDs, causing transcriptional activation of fatty acid biosynthesis and metabolic reprogramming to glycolysis. Heme oxygenase (HO)-1 counteracts CLP-mediated septic shock in mouse models. In HO-1-deficient mice, LD formation was not observed upon CLP, but a concomitant decrease in "LD-decorating proteins" was observed, implying a link between LDs and cytoprotective activity. Collectively, LD biogenesis during stress can trigger adaptive LD formation, which is dependent on mitochondrial integrity and HO-1 activity; this may be a cellular survival strategy, apportioning energy-generating substrates to cellular defense. 

Retracted: No

PubPeer comments:
 c and d show the same object ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Long Non-Coding RNA CASC9 And HIF-1α Form A Positive Feedback Loop To Facilitate Cell Proliferation And Metastasis In Lung Cancer
Authors: Deping Zhao
Huikang Xie
Gening Jiang
Yuxing Jin
Jiaan Ding
Liang Duan
Journal: OncoTargets and therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: CASC9; HIF-1α; cell proliferation; lung cancer; metastasis.
Affiliations: Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, People's Republic of China.

Abstract:  Background: The long noncoding RNA cancer susceptibility 9 (CASC9) has been recognized as an important modulator of cell growth and metastasis in many cancers. However, its detailed roles in lung cancer remain unclear. In this study, we aimed to investigate its functions and molecular mechanism in lung cancer progression. Methods: Expression of CASC9 was determined in lung cancer tissues and cell lines by real-time PCR. CCK-8, colony formation, wound healing and transwell assays were done to evaluate the cell proliferation, migration and invasion capacities in vitro. Real-time PCR, Western blot and RNA immunoprecipitation (RIP) assays were performed to dissect the mechanisms. Results: CASC9 was overexpressed in lung cancer specimens and cell lines. Knockdown of CASC9 inhibited cell proliferation, migration, invasion and EMT in lung cancer cells. While overexpression of CASC9 in normal lung epithelial cells did the opposite. CASC9 interacted with HIF-1α and enhanced its protein stability. They formed a positive feedback loop by reciprocally inducing each other expression and regulated cell proliferation and metastasis. Conclusion: Our findings demonstrated a novel regulatory signaling pathway, namely the CASC9/HIF-1α axis, which was involved in lung cancer progression. These findings can provide valuable insights on the potential therapy application for lung cancer. 

Retracted: No

PubPeer comments:
 Figure 5D appears to contain repeated images. *** ![file] ,
Ischemic Duration and Frequency Determines AKI-to-CKD Progression Monitored by Dynamic Changes of Tubular Biomarkers in IRI Mice
Authors: Li He
Jianyong Yin
Niansong Wang
Qunzi Zhang
Shiqi Li
Yang Dong
Teng Chen
Ying Fan
Yiyun Wang
Rui Wu
Jiejun Wen
Rui Xue
Journal: Frontiers in Physiology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: KIM-1; NGAL; acute kidney injury; chronic kidney disease; ischemia-reperfusion injury.
Affiliations: Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Abstract:  Ischemia reperfusion injury (IRI) is one of the most common causes of acute kidney injury (AKI). However, the pathogenesis and biomarkers predicting the progression of IRI-induced AKI to chronic kidney disease (CKD) remain unclear. A side-by-side comparison between different IRI animal models with variable ischemic duration and episodes was performed. The dynamic changes of KIM-1 and NGAL continuously from AKI to CKD phases were studied as well. Short-term duration of ischemia induced mild renal tubule-interstitial injury which was completely reversed at acute phase of kidney injury, while long-term duration of ischemia caused severe tubular damage, cell apoptosis and inflammatory infiltration at early disease stage, leading to permanent chronic kidney fibrosis at the late stage. Repeated attacks of moderate IRI accelerated the progression of AKI to CKD. Different from serum and urine levels of KIM-1 that increased at acute phase of IRI then declined gradually in chronic phase, NGAL increased continuously during AKI-to-CKD transition. Severity and frequency of ischemia injury determines the progression and outcome of ischemia-induced AKI. Inflammation, apoptosis and fibrogenesis likely participate in the progression of AKI to CKD. Both KIM-1 and NGAL enable noninvasive and early detection of AKI, but NGAL is associated better with the process of AKI-to-CKD progression. 

Retracted: No

PubPeer comments:
 Images in Figure 1A and 2A appear to overlap, after adjusting color. *** ![file] , 
 Images in Figure 3A appear to overlap. *** ![file] , 
 Images within Figure 2A appear to overlap (red and green boxes), after recoloring. These errors are difficult to explain as merely errors made during figure assembly. This and other features in this paper are sometimes seen in paper mill (or outsourced) papers. TAM. *** ![file] ,
Genetic Deletion of Prostacyclin IP Receptor Exacerbates Transient Global Cerebral Ischemia in Aging Mice
Authors: Sofiyan Saleem
Hania Shakil
Journal: Brain Sciences (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: aging; cognitive deficit; global cerebral ischemia; mouse; prostaglandin I2.
Affiliations: Hamdard College of Medicine and Dentistry, Hamdard University, Sharae Madinat Al-Hikmah, Karachi 74600, Pakistan., Center for Neuroscience, Aging and Stem Cell Research, Sanford Burnham Medical Research Institute, La Jolla, CA 92037, USA.

Abstract:  Transient global cerebral ischemia causes delayed neuronal death in the hippocampal CA1 region. It also induces an up regulation of cyclooxygenase 2 (COX-2), which generates several metabolites of arachidonic acid, known as prostanoids, including Prostaglandin I2 (PGI2). The present study investigated whether the PGI2 IP receptor plays an important role in brain injury after global cerebral ischemia in aged mice. Adult young (2-3 months) and aged (12-15 months) male C57Bl/6 wild-type (WT) or IP receptor knockout (IP KO) mice underwent a 12 min bilateral common carotid artery occlusion (BCCAO) or a sham surgery. Behavior tests (neurologic deficit and T-maze) were performed 3 and 7 days after BCCAO. After seven days of reperfusion, the numbers of cells positive for markers of neurons, astrocytes, microglia, myeloperoxidase (MPO) and phosphorylated CREB (p-CREB) were evaluated immunohistochemically. Interestingly, in young and aged IP KO ischemic mice, there was a significant increase (p &lt; 0.01) in cognitive deficit, hippocampal CA1 pyramidal neuron death, microglia and MPO activation, while p-CREB was reduced as compared to their corresponding WT controls. These data suggest that following ischemia, IP receptor deletion contributes to memory and cognitive deficits regulated by the CREB pathway and that treatment with IP receptor agonists could be a useful target to prevent harmful consequences. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. , 
 We are highly thankful for providing valuable comment on the research paperu201d Genetic Deletion of Prostacyclin IP receptor Exacerbates Transient Global Cerebral Ischemia in Aging Mice. Brain Sci. 2013 Jul 22,3 (3):1095-108 on pub peer website. We corrected the identical representative images in Figure 7 as reported in pub peer comment and submitted to the brain Sciences journal as correction notice draft. I hope these changes have no material impact on the conclusions of our research article. In addition, this research work will help to find a new therapeutic target and drugs to find a cure against this devastating diseases such as cardiac arrest and stroke especially against aging population. Paper Author ,
Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro
Authors: Yang-Lin Wei
Li-Na Wang
Xuan Wang
Zi-Fei Yin
Xia Li
Journal: BMC Complementary Medicine and Therapies (2020)
Discipline: CLINICAL MEDICINE
Keywords: A549 cells; Akt; Buyang Huanwu Tang; PI3K; Pulmonary fibrosis.
Affiliations: Department of Traditional Chinese Medicine, Changhai Hospital, The Second Military Medical University, No.168 Changhai Road, Shanghai, 200433, China., Department of Traditional Chinese Medicine, Changhai Hospital, The Second Military Medical University, No.168 Changhai Road, Shanghai, 200433, China. .

Abstract:  Background: Pulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease. Buyang Huanwu Tang (BYHWT), a classical traditional Chinese medicine formula, has been widely utilized for the treatment of PF in China. This present study aimed to explore the mechanism of BYHWT in the treatment of PF in vitro. Methods: TGF-β1 stimulated human alveolar epithelial A549 cells were used as in vitro model for PF. Post the treatment of BYHWT, cell viability was measured by MTT assay, and cell morphology was observed under microscope. The epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, Vimentin) and collagen I (Col I) were detected by western blot, immunofluorescence staining and real-time quantitative polymerase chain reaction. With the co-administration of activators (IGF-1, SC79) and inhibitors (LY294002, MK2206), the effect of BYHWT on PI3K/Akt pathway was analyzed by western blot. Results: BYHWT inhibited cell growth, and prevented cell morphology changed from epithelial to fibroblasts in TGF-β1 induced A549 cells. BYHWT decreased Vimentin and Col I, while increased E-cadherin at both protein and mRNA levels. Moreover, phosphorylation of PI3K (p-PI3K) and phosphorylation of Akt (p-Akt) were significantly down-regulated by BYHWT in TGF-β1 stimulated A549 cells. Conclusion: These results indicate that BYHWT suppressed TGF-β1-induced collagen accumulation and EMT of A549 cells by inhibiting the PI3K/Akt signaling pathway. These findings suggest that BYHWT may have potential for the treatment of PF. 

Retracted: No

PubPeer comments:
 Figure 4. * Yellow boxes: The E-cadherin - - panel appears to show a large overlap with the Vimentin + - panel. Note that the red signal appears to differ between these two. ![file] ,
CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling
Authors: Nan Wang
Xiaochun Wang
Zhuo Chen
Mingli Han
Lin Li
Yuanting Gu
Fang Wang
Jingruo Li
Pengwei Lv
Lingling Dong
Journal: Journal of Biomedical Science (2021)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer; Circular RNA; JAK/STAT signaling; SOCS2; circNOL10
Affiliations: Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Erqi, Zhengzhou, 450000, China., Department of Breast Surgery, Affiliated Hospital of Hebei University, Baoding, 071000, China., Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Erqi, Zhengzhou, 450000, China. .

Abstract:  Background: Circular RNAs (circRNAs) have caught increasing attentions and interests for their important involvement in cancer initiation and progression. This study aims to investigate the biological functions of circNOL10 and its potential molecular mechanisms in breast cancer (BC). Materials and methods: qRT-PCR and western blot assays were performed to measure the expression of related genes. CCK-8, colony formation, flow cytomerty and transwell assays were used to assess cell proliferation, cell cycle, migration and invasion. RNA pull-down, luciferase reporter and RIP assays were applied to address the potential regulatory mechanism of circNOL10. Results: CircNOL10 was down-regulated in BC tissues and cells. Low expression of circNOL10 was associated with larger tumor size, advanced TNM stage, lymph node metastasis and unfavorable prognosis. Overexpression of circNOL10 inhibited cell proliferation, migration, invasion and EMT in vitro and slowed xenograft tumor growth in vivo. Mechanistically, circNOL10 could act as a molecular sponge for miR-767-5p, leading to the up-regulation of suppressors of cytokine signaling 2 (SOCS2) and inactivation of JAK2/STAT5 pathway. Moreover, circNOL10-mediated suppression of malignant phenotypes was attenuated by miR-767-5p. Similar to circNOL10, enforced expression of SOCS2 also resulted in the suppression of cell proliferation and metastasis. Furthermore, knockdown of SOCS2 reversed the tumor-suppressive effect induced by circNOL10. Conclusions: CircNOL10 repressed BC development via inactivation of JAK2/STAT5 signaling by regulating miR-767-5p/SOCS2 axis. Our findings offer the possibility of exploiting circNOL10 as a therapeutic and prognostic target for BC patients. 

Retracted: No

PubPeer comments:
 The Western immuno blots in Figure 4 and 5 look odd. Diffuse bands with strange background pattern in Figure 4 and lack of background vs background noise in Figure 5. ![file] ,
The characteristics of bone marrow-derived endothelial progenitor cells and their effect on glioma
Authors: You-Yi Lu
She-Hong Zhang
He-Yong Wang
Hao Jiang
Yan-Li Luo
Ping Xiang
Journal: Cancer Cell International (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EPCs; bone marrow; angiogenesis; endothelium; tumor vessels
Affiliations: Center for Laboratory Research, First Affiliated Hospital of Bengbu Medical College, Anhui 233004, China. .

Abstract:  Background: EPCs were isolated primarily in 1997 by Asahara et al. and recent studies indicated that bone-marrow-derived EPCs contributed little to the endothelium of tumor vessels. Tumors of the CNS system demonstrate various features of angiogenesis. Methods: EPCs derived from rat bone marrow were isolated and cultured in M199 medium without any induced factors. EPCs were studied using immunohistochemical staining, Flow cytometry and culture under three-dimensional condition to determine EPCs' characteristics in vitro. We also established an animal model by injecting EPCs marked with Hoechst 33342 into the back of BALB/c nude mice and performed hematoxylin-eosin (HE) and immunofluorescent staining to study EPCs' features in vivo. To research effect of EPCs on glioma, animals bearing tumors model with C6 glioma were established. About 27 day after injection, we performed immunohistochemical staining and Immunofluorescence staining. Results: Our results showed that EPCs derived from rat bone marrow appeared typical morphological characteristics and were positive of CD34, CD133, KDR and CD31 antigens at different time in vitro under the special M199 medium without any induced factors. The percentage of cells that expressed CD133 decreased gradually. In brief, the present study showed that EPCs derived from rat bone marrow differentiated into ECs in medium the without any induced factors and formed tubular structures in three-dimensional circumstances. Animal experiments suggested that EPCs differentiated into ECs and other else non-endothelial cells, and that EPCs contributed M199 of glioma. Discussion: These findings provides some novel results about biological characteristics of EPCs in vivo and ex vivo, and an update on the effect of EPCs on glioma and which would be helpful for the overall understanding of EPCs and make EPCs to be implied on the clinical therapy. 

Retracted: No

PubPeer comments:
 image duplication repositioned ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Dynamic real-time imaging of living cell traction force by piezo-phototronic light nano-antenna array
Authors: Weiguo Hu
Rongcheng Han
Zhong Lin Wang
Qiang Zheng
Mingzeng Peng
Han Ouyang
Zhuo Liu
Shuyu Li
Caofeng Pan
Yubo Fan
Junyi Zhai
Zhou Li
Journal: Science Advances (2021)
Discipline: Multidisciplinary
Keywords: force mapping; cardiomyocytes; piezo-phototronic effect; spatial resolution; temporal resolution
Affiliations: CAS Center for Excellence in Nanoscience, Beijing Key Laboratory of Micro-Nano Energy and Sensor, Beijing Institute of Nanoenergy and Nanosystems, Chinese Academy of Sciences, 100083 Beijing, China., Beijing Advanced Innovation Center for Biomedical Engineering, Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, 100191 Beijing, China., Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, 100101 Beijing, China., School of Nanoscience and Technology, University of Chinese Academy of Sciences, 100049 Beijing, China., School of Materials Science and Engineering, Georgia Institute of Technology, Atlanta, GA 30332-0245, USA.

Abstract:  Dynamic mapping of the cell-generated force of cardiomyocytes will help provide an intrinsic understanding of the heart. However, a real-time, dynamic, and high-resolution mapping of the force distribution across a single living cell remains a challenge. Here, we established a force mapping method based on a "light nano-antenna" array with the use of piezo-phototronic effect. A spatial resolution of 800 nm and a temporal resolution of 333 ms have been demonstrated for force mapping. The dynamic mapping of cell force of live cardiomyocytes was directly derived by locating the antennas' positions and quantifying the light intensities of the piezo-phototronic light nano-antenna array. This study presents a rapid and ultrahigh-resolution methodology for the fundamental study of cardiomyocyte behavior at the cell or subcellular level. It can provide valuable information about disease detection, drug screening, and tissue engineering for heart-related studies. 

Retracted: No

PubPeer comments:
 Typo on  The key concept of the piezo-phototronic effect is using stain-generated piezoelectric polarization charges  -  strain-generated . The article later talks about strain in this context. ,
Express penetration of hydrogen on Mg(10͞13) along the close-packed-planes
Authors: Min Zhu
Xiangdong Yao
Jiajun Tang
Liuzhang Ouyang
Jin Zou
Yujun Zhao
Jiangwen Liu
Hui Wang
Journal: Scientific reports (2015)
Discipline: Multidisciplinary
Keywords: Metal atoms; close-packed planes; high-index planes; hydrogen penetration; diffusion
Affiliations: 1] School of Materials Science and Engineering, Key Laboratory of Advanced Energy Storage Materials of Guangdong Province, South China University of Technology, Guangzhou, 510641, People's Republic of China [2] China-Australia Joint Laboratory for Energy & Environmental Materials, South China University of Technology, Guangzhou, 510641, PR China., 1] School of Materials Science and Engineering, Key Laboratory of Advanced Energy Storage Materials of Guangdong Province, South China University of Technology, Guangzhou, 510641, People's Republic of China [2] Department of Physics, South China University of Technology, Guangzhou 510640, People's Republic of China [3] China-Australia Joint Laboratory for Energy & Environmental Materials, South China University of Technology, Guangzhou, 510641, PR China., 1] Department of Physics, South China University of Technology, Guangzhou 510640, People's Republic of China [2] China-Australia Joint Laboratory for Energy & Environmental Materials, South China University of Technology, Guangzhou, 510641, PR China., School of Biomolecular and Physical Sciences, Griffith University, Nathan, QLD 4111, Australia., Materials Engineering and Centre for Microscopy and Microanalysis, The University of Queensland, St. Lucia, QLD 4072, Australia.

Abstract:  Metal atoms often locate in energetically favorite close-packed planes, leading to a relatively high penetration barrier for other atoms. Naturally, the penetration would be much easier through non-close-packed planes, i.e. high-index planes. Hydrogen penetration from surface to the bulk (or reversely) across the packed planes is the key step for hydrogen diffusion, thus influences significantly hydrogen sorption behaviors. In this paper, we report a successful synthesis of Mg films in preferential orientations with both close- and non-close-packed planes, i.e. (0001) and a mix of (0001) and (10͞13), by controlling the magnetron sputtering conditions. Experimental investigations confirmed a remarkable decrease in the hydrogen absorption temperature in the Mg (10͞13), down to 392 K from 592 K of the Mg film (0001), determined by the pressure-composition-isothermal (PCI) measurement. The ab initio calculations reveal that non-close-packed Mg(10͞13) slab is advantageous for hydrogen sorption, attributing to the tilted close-packed-planes in the Mg(10͞13) slab. 

Retracted: No

PubPeer comments:
 Figure 2 shows some repetitions in noise. Not sure I found all of it. ![file] ,
Intestinal involvement during 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced chronic liver injury in a mouse model
Authors: Karl G Sylvester
Unsal Kuscuoglu
Banu Altindag
Guo-Zhong Tao
Nadja Lehwald
Igor Sukhotnik
Journal: Journal of Pediatric Surgery (2011)
Discipline: CLINICAL MEDICINE
Keywords: intestinal mucosal integrity; hepatic function; primary liver disease; chronic liver injury; enterocyte turnover
Affiliations: Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. 

Abstract:  Purpose: Although a physiologic relationship between intestinal mucosal integrity and hepatic function has been previously described, the effect of primary liver disease on intestinal mucosal homeostasis has not been previously well documented. In the current study, we studied the effects of chronic liver injury as a primary injury on enterocyte turnover (proliferation and apoptosis) in a mouse model. Methods: The liver toxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-enriched diet was used to induce chronic cholestatic liver injury in mice. Livers and intestine were harvested after 3 weeks of dietary treatment of histologic analysis and a determination of cell proliferation (immunohistochemistry for Ki67), or apoptosis (immunohistochemistry for caspase-3), as well as a determination of Wnt/β-catenin signaling activity. Results: All DDC-fed animals exhibited histologic evidence of liver damage that was associated with the expansion of atypical ductal proliferation near the periportal areas and increased oxidative stress. In the intestine, DDC-induced liver damage was associated with decreased villus height, decreased enterocyte proliferation, and increased cell apoptosis compared with control animals. There was also evidence for decreased β-catenin expression by immunostaining in crypt and villus cells of DDC-fed mice compared with control animals. Conclusion: Primary liver injury and cholestasis is associated with intestinal mucosal hypoplasia. Decreased cell proliferation and increased cell apoptosis may be responsible for decreased intestinal epithelial cell mass. The observed decrease in cell turnover is accompanied by an alteration in Wnt/β-catenin signaling. 

Retracted: No

PubPeer comments:
 Figure 5. * Blue and green boxes: the panels here (representing mouse tissues) look very similar to panels in another paper by the same first author, where they represent rat tissues. That paper is: Sukhotnik et al., Pediatr Surg Int (2014) 30:173u2013180, DOI: 10.1007 s00383-013-3447-9 - https: pubpeer.com publications 879E4B742935C9EEAB4A8B05A3733D ![file] ,
MiR-155 regulates oral squamous cell carcinoma Tca8113 cell proliferation, cycle, and apoptosis via regulating p27Kip1
Authors: Y Wu
P Cheng
H-H Chen
S Fu
C-B Zhang
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: P27Kip1; cell cycle; cell proliferation; oral squamous cell carcinoma (OSCC); miR-155
Affiliations: Department of Oral and Maxillofacial Surgery, the Affiliated Stomatology Hospital of Kunming Medical University, Yunnan, Kunming, China. .

Abstract:  Objective: P27Kip1 is the one of the negative regulators of the cell cycle that plays an important role in regulating cell cycle and inhibiting cell proliferation by restraining cell in G1 phase. P27Kip1 downregulation maybe related to the occurrence of oral squamous cell carcinoma (OSCC). It was found that miR-155 significantly upregulated in OSCC tissue. Bioinformatics analysis revealed that miR-155 may bind with the 3'-UTR of p27Kip1. This study investigated the role of miR-155 in regulating p27Kip1 and affecting Tca8113 cell proliferation, cycle, and apoptosis. Patients and methods: A total of 46 cases of OSCC patients received treatment in our hospital were enrolled to obtain tumor tissue. Another 25 normal oral mucosa samples were selected as control to detect the relationship between miR-155 and p27Kip1 expressions. Dual luciferase assay was adopted to confirm the targeted relationship between miR-155 and p27Kip1. Flow cytometry was applied to test cell apoptosis and cell cycle. CCK-8 assay was used to evaluate cell proliferation. Caspase-3 activity was detected by spectrophotometry. Results: MiR-155 upregulated, while p27Kip1 declined in OSCC tissue compared with normal oral mucosa. Their expressions were related to TNM stage. MiR-155 targeted suppressed p27Kip1 expression. MiR-155 mimic and/or pEGFP-p27Kip1 transfection obviously declined p27Kip1 expression, blocked cell cycle in G1 phase, reduced cell proliferation, enhanced Caspase-3 activity, and increased cell apoptosis in Tca8113 cells. Conclusions: MiR-155 increased, while p27Kip1 reduced in OSCC tissue. Inhibition of miR-155 upregulated p27Kip1 expression, blocked cell cycle in G1 phase, weakened cell proliferation, and induced cell apoptosis. 

Retracted: No

PubPeer comments:
 This paper has features suggestive of [what has elsewhere been labeled as  Papermill #2 ] , characterised by stylised geometrical Western Blots that are reduced to black blobs on a featureless grey background, reminiscent of a Miro painting: ![file] ...and by a small repertoire of recurring flow cytometry plots, ![file] slightly modified by artisanal stippling on each of their occurrences. ![] Other examples are listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit?usp=sharing ,
Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase
Authors: David Carling
Odile D Peroni
Yasuhiko Minokoshi
Young-Bum Kim
Lee G D Fryer
Barbara B Kahn
Corinna Müller
Journal: Nature (2002)
Discipline: Multidisciplinary
Keywords: Leptin; adipocytes; food intake; energy expenditure; neuroendocrine function
Affiliations: Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

Abstract:  Leptin is a hormone secreted by adipocytes that plays a pivotal role in regulating food intake, energy expenditure and neuroendocrine function. Leptin stimulates the oxidation of fatty acids and the uptake of glucose, and prevents the accumulation of lipids in nonadipose tissues, which can lead to functional impairments known as "lipotoxicity". The signalling pathways that mediate the metabolic effects of leptin remain undefined. The 5'-AMP-activated protein kinase (AMPK) potently stimulates fatty-acid oxidation in muscle by inhibiting the activity of acetyl coenzyme A carboxylase (ACC). AMPK is a heterotrimeric enzyme that is conserved from yeast to humans and functions as a 'fuel gauge' to monitor the status of cellular energy. Here we show that leptin selectively stimulates phosphorylation and activation of the alpha2 catalytic subunit of AMPK (alpha2 AMPK) in skeletal muscle, thus establishing a previously unknown signalling pathway for leptin. Early activation of AMPK occurs by leptin acting directly on muscle, whereas later activation depends on leptin functioning through the hypothalamic-sympathetic nervous system axis. In parallel with its activation of AMPK, leptin suppresses the activity of ACC, thereby stimulating the oxidation of fatty acids in muscle. Blocking AMPK activation inhibits the phosphorylation of ACC stimulated by leptin. Our data identify AMPK as a principal mediator of the effects of leptin on fatty-acid metabolism in muscle. 

Retracted: No

PubPeer comments:
null, 
 Do the authors have an explanation for the duplicated bands? , 
null, 
null, 
 The clearly duplicated lanes in figure 3c were pointed out 2 years ago. Could the authors explain how likely that is to occur by chance? So far no response. , 
 #5 * Could the authors explain how likely that is to occur by chance? So far no response. * There is no guarantee that the authors were ever alerted to this discussion. The e-mail address published with this 17-year old paper seems no longer current. Did you attempt to add any author e-mails via this page? I don t see any check marks next to the author names. I will add a current address for the last author from 2018-2019 papers. Whether any authors can shed light on these old gels is another matter entirely... ,
Long noncoding RNA AFAP1-AS1 accelerates the proliferation and metastasis of prostate cancer via inhibiting RBM5 expression
Authors: Z-T Yang
J-D Hu
F An
W-H Zhao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; AFAP1-AS1; prostate cancer; cell proliferation; metastasis
Affiliations: Department of Urology, Longnan Hospital, Daqing, China. .

Abstract:  Objective: Recently, the role of long noncoding RNA (lncRNAs) in tumor progression has caught many attentions. In this research, lncRNA AFAP1-AS1 was studied to identify how it functioned in the progression of prostate cancer. Patients and methods: LncRNA AFAP1-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both prostate cancer cells and tissue samples. In addition, to identify the function of AFAP1-AS1 on prostate cancer in vitro, cell proliferation, transwell assay, and Matrigel assay were conducted. Furthermore, by performing qRT-PCR and Western blot assay, the underlying mechanism was explored. Results: The expression level of AFAP1-AS1 was significantly higher in prostate cancer samples than that in corresponding ones. Additionally, the cell proliferation, migration, and invasion capacities were inhibited after AFAP1-AS1 was knocked down in prostate cancer cells. Moreover, the mRNA and protein expressions of RBM5 were upregulated after AFAP1-AS1 was knocked down. Furthermore, the RBM5 expression level was negatively related to AFAP1-AS1 expression level in prostate cancer samples. Conclusions: AFAP1-AS1 acts as an oncogene in prostate cancer by enhancing cell metastasis and proliferation via suppressing RBM5, which might be a novel therapeutic strategy in treatment for prostate cancer. 

Retracted: No

PubPeer comments:
 This paper is one of a set of 121 papers that all contain images from the same library of about 100 photos and plots. This is unexpected, because each paper has different authors and different affiliations, with little to no overlap, and describes different cancer types and molecules. It would be very hard to explain how authors from different labs would all obtain the same photo. Therefore, the papers might have all be derived from the same source, such as a paper mill that sells ready-to-be-published papers. This  Stock Photo paper set has been described in more detail on my blog post, https: scienceintegritydigest.com 2020 07 05 the-stock-photo-paper-mill and in a Wall Street Journal article by Eva Xiao (currently behind a paywall): https: www.wsj.com articles chinese-research-papers-raise-doubts-fueling-global-questions-about-scientific-integrity-11593939600 The vast majority (113 121) of the papers were published in the same journal, European Review for Medical and Pharmacological Sciences (ERMPS). A link to the full set of papers can be found here: https: docs.google.com spreadsheets d 172RWS18w1lTNJ9Nnj80fuXXTqTm4fGkoK0sdYyvKE3g edit?usp=sharing All papers have been reported to the journal editors on July 2, 2020. ,
Synthesis of a novel glycoconjugated chitosan and preparation of its derived nanoparticles for targeting HepG2 cells
Authors: Shu-Huei Yu
Mei-Chin Chen
Hsing-Wen Sung
Yong-Yi Wu
Mei-Feng Huang
Ya-Lin Chiu
Shin-Shing Shyu
Fwu-Long Mi
Journal: Biomacromolecules (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Chitosan; Galactose; Nanoparticles; Hepatoma cells; Targeting
Affiliations: Department of Biotechnology, Vanung University, Chung-Li, Taiwan, Republic of China, Department of Chemical Engineering, National Tsing Hua University, Hsinchu, Taiwan, Republic of China, Department of Polymer Materials, Vanung University, Chung-Li, Taiwan, Republic of China, Nano Materials R&D Center, Vanung University, Chung-Li, Taiwan, Republic of China, and Department of Chemical and Material Engineering, National Central University, Chung-Li, Taiwan, Republic of China

Abstract:  In the study, a novel chitosan (CS) derivative conjugated with multiple galactose residues in an antennary fashion (Gal-m-CS) was synthesized. A galactosylated CS (Gal-CS) was also prepared by directly coupling lactobionic acid on CS. Using an iontropic gelation method, CS and the synthesized Gal-CS and Gal-m-CS were used to prepare nanoparticles (CS, Gal-CS, and Gal-m-CS NPs) for targeting hepatoma cells. TEM examinations showed that the morphology of all three types of NPs was spherical in shape. No aggregation or precipitation of NPs in an aqueous environment was observed during storage for all studied groups, as a result of the electrostatic repulsion between the positively charged NPs. Little fluorescence was observed in HepG2 cells after incubation with the FITC-labeled CS NPs. The intensity of fluorescence observed in HepG2 cells incubated with the Gal-m-CS NPs was stronger than that incubated with the Gal-CS NPs. These results indicated that the prepared Gal-m-CS NPs had the highest specific interaction with HepG2 cells among all studied groups, via the ligand-receptor-mediated recognition. 

Retracted: No

PubPeer comments:
 ![file] Figure 4. The 2 size distribution profiles look highly similar , 
 ![file] It could be a coincidence but some particles in Figure 5 share similarities. , 
 #1 Raw data from Zetasizer: ![file] ![file] Intensity: same Size, volume and number: different #2 See the edge of each block (1-8) ![file] Fwu-Long Mi , 
 #1 The size distribution is *somewhat* different. Still, the two distributions are surprisingly similar. The bins are not sitting in the same position but their heights are near-identical. This seems odd. [ click to animate, Gal-CS and Gal-m-CS ] ![file] , 
 #2 I recognize your concern. In fact, the figure may contain one particle duplicated 5 times. This seems very co-incidental for a particles particles that is are not round. [ Click to animate. Rotate -50 degrees, scale by -4% ] ![file] [ Click to animate. Simple shift ] ![file] [ Click to animate. Simple shift ] ![file] [ Click to animate. Rotate -95 degrees, scale by -18% ] ![file] ,