PReD-Bench/PRed-Bench huggingface dataset:
Deconvolution of Voltage Sensor Time Series and Electro-diffusion Modeling Reveal the Role of Spine Geometry in Controlling Synaptic Strength
Authors: Taekyung Kwon
Jerome Cartailler
David Holcman
Rafael Yuste
Journal: Neuron (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Electro-diffusion; deconvolution; dendritic spines; fluorescent signal; mathematical modeling
Affiliations: Institut de Biologie de l'École Normale Supérieure, 46 rue d'Ulm, 75005 Paris, France., Neurotechnology Center, Depts. Biological Sciences and Neuroscience, Columbia University, New York, NY 10027, USA., Institut de Biologie de l'École Normale Supérieure, 46 rue d'Ulm, 75005 Paris, France. Electronic address: .

Abstract:  Most synaptic excitatory connections are made on dendritic spines. But how the voltage in spines is modulated by its geometry remains unclear. To investigate the electrical properties of spines, we combine voltage imaging data with electro-diffusion modeling. We first present a temporal deconvolution procedure for the genetically encoded voltage sensor expressed in hippocampal cultured neurons and then use electro-diffusion theory to compute the electric field and the current-voltage conversion. We extract a range for the neck resistances of 〈R〉=100±35MΩ. When a significant current is injected in a spine, the neck resistance can be inversely proportional to its radius, but not to the radius square, as predicted by Ohm's law. We conclude that the postsynaptic voltage cannot only be modulated by changing the number of receptors, but also by the spine geometry. Thus, spine morphology could be a key component in determining synaptic transduction and plasticity. 

Retracted: No

PubPeer comments:
 https: referee3.org 2018 08 24 one-equation-two-unknowns ,
CDC27 Promotes Tumor Progression and Affects PD-L1 Expression in T-Cell Lymphoblastic Lymphoma
Authors: Zhaoming Li
Qingxin Xia
Wei Song
Mingzhi Zhang
Jiwei Li
Yue Song
Yibo Wen
Wenting Song
Journal: Frontiers in Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: APC/C; CDC27; PD-L1; T-cell lymphoblastic lymphoma; cell cycle.
Affiliations: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China., The Academy of Medical Science of Zhengzhou University, Zhengzhou, China., Lymphoma Diagnosis and Treatment Center of Henan Province, Zhengzhou, China., Department of Pathology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, China.

Abstract:  T-lymphoblastic lymphoma (T-LBL) is a rare hematological malignancy with highly aggressive, unique clinical manifestations, and poor prognosis. Cell division cycle 27 (CDC27) was previously reported to be a significant subunit of the anaphase-promoting complex/cyclosome. However, the specific functions and relevant mechanisms of CDC27 in T-LBL remain unknown. Through immunohistochemistry staining, we identified that CDC27 was overexpressed in T-LBL tissues and related to tumor progression and poor survival. Functional experiments demonstrated that CDC27 promoted proliferation in vivo and in vitro. Further experiment suggested the role of CDC27 in facilitating G1/S transition and promoting the expression of Cyclin D1 and CDK4. Then the effect of CDC27 in inhibiting apoptosis was also identified. Furthermore, we found a positive correlation between the expression of CDC27 and Programmed death ligand-1 (PD-L1) by immunohistochemistry staining. The interaction between CDC27 and PD-L1 was also proved by western blot, luciferase gene reporter assay and immunofluorescence. Taken together, our results showed that CDC27 contributes to T-LBL progression and there is a positive correlation between PD-L1 and CDC27, which offers novel perspectives for future studies on targeting CDC27 in T-LBL. 

Retracted: No

PubPeer comments:
 In Figure 3A and Figure 4A,B, flow cytometry dot plots have been duplicated and presented as something else and the values are different. ![file] ,
Assesment the role of oxidative stress and efficacy of caffeic acid phenethyl ester (CAPE) on neurotoxicity induced by isoniazid and ethambutol in a rat model
Authors: O Evliyaoglu
Y Yucel
S Varol
H Alp
S K Basarslan
E Uzar
O Gökalp
U Firat
A Acar
Journal: European review for medical and pharmacological sciences (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: oxidative stress; caffeic acid phenethyl ester (CAPE); neurotoxicity; isoniazid; ethambutol
Affiliations: Department of Neurology, School of Medicine, Dicle University, Diyarbakir, Turkey.   

Abstract:  Objective: The aim of this study were to investigate a role of oxidative stress and the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) in the pathogenesis of neurotoxicity induced by isoniazid and etambutol in a rat model. Materials and methods: Male Sprague-Dawley rats were randomly divided into eight experimental groups: control, INH, ETM, INH+ETM, INH+CAPE, ETM+CAPE, INH+ETM+CAPE, and CAPE treatment group, with ten animals in each group. INH and ETM doses were given orally within tap water for 30 days. CAPE was administered into relevant groups intraperitoneally for 30 days. Brain tissue and sciatic nerve were removed for biochemical and histopathological investigation. Results: In the INH, ETM, and INH+ETM groups, malondialdehyde (MDA) and total oxidant status (TOS) levels were significantly higher than those of the control group (p &lt; 0.05). Also, in these groups, brain total antioxidant capacity (TAC) levels, and superoxide dismutase (SOD) and PON-1 activities were decreased compared with the control group (p &lt; 0.05). By a CAPE supplement within INH and ETM groups, there was a significant decrease in MDA and TOS (p &lt; 0.05). In addition to a significant increase in TAC levels, and SOD and PON-1 activities both in brain and sciatic nerve tissues (p &lt; 0.05). Conclusions: CAPE may protect against INH- and ETM-induced neurotoxicity in rat brain and sciatic nerve. 

Retracted: No

PubPeer comments:
 Figure 1. * Blue boxes: Panels B (ETM group) and C (INH+ETM group) appear to look identical. ![file] ,
<p>MicroRNA-188-5p Promotes Epithelial–Mesenchymal Transition by Targeting ID4 Through Wnt/β-catenin Signaling in Retinoblastoma</p>
Authors: Ming Yang
Wenbin Wei
Yang Li
Journal: OncoTargets and Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: ID4; Wnt/β catenin signaling; epithelial-mesenchymal transition; miRNA-188-5p; retinoblastoma.
Affiliations: Beijing Tongren Eye Center, Beijing Key Laboratory of Intraocular Tumor Diagnosis and Treatment, Beijing Ophthalmology & Visual Sciences Key Lab, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, People's Republic of China.

Abstract:  Purpose: Here, we investigated the involvement of the miR-188-5p/inhibitor of the DNA binding 4 (ID4) axis in retinoblastoma (Rb). Patients and methods: We included 35 Rb tissues and the corresponding adjacent normal tissues. RT-qPCR, Western blot, lentivirus transfection, measurement of cell migration in vitro, and chip analysis were performed during the study. Mouse Rb models were established to investigate the in vivo mechanisms. Results: We showed that miR-188-5p was upregulated in Rb tissues; moreover, we identified a pathway involving the upregulation of miR-188-5p and its downstream target, ID4, in vitro. Cell experiments revealed that the overexpression of miR-188-5p significantly downregulated the expression of ID4 and the underlying mechanism involved direct targeting of the ID4 3'-UTR. The levels of ID4 are lower in Rb tissues; it plays an antitumor role by inhibiting Rb metastasis in vitro and in vivo. Further investigation revealed that the miR-188-5p/ID4 axis regulated metastasis by promoting epithelial-mesenchymal transition (EMT). We demonstrated that microRNA-188-5p promoted EMT by targeting ID4 through Wnt/β catenin signaling in Rb. Conclusion: miRNA-188-5p can promote EMT by targeting ID4 through the Wnt/β‑catenin signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 3G and Figure 3H ![file] ,
Simvastatin Strongly Augments Proapoptotic, Anti-inflammatory and Cytotoxic Activity of Oxicam Derivatives in Doxorubicin-resistant Colon Cancer Cells
Authors: Anna Uryga
Anna Palko-Łabuz
Berenika Szczęśniak-Sięga
Krystyna Michalak
Kamila Środa-Pomianek
Olga Wesołowska
Journal: Anticancer research (2019)
Discipline: CLINICAL MEDICINE
Keywords: Oxicam derivatives; apoptosis; cancer combination therapy; cyclo-oxygenase-2; simvastatin.
Affiliations: Department of Biophysics, Wroclaw Medical University, Wroclaw, Poland ., Department of Biophysics, Wroclaw Medical University, Wroclaw, Poland., Department of Chemistry of Drugs, Wroclaw Medical University, Wroclaw, Poland.

Abstract:  Background: Incidence of cancer is still increasing. Chemotherapy is often unsuccessful; moreover, anticancer drugs cause serious side-effects. It is necessary to develop effective agents for combination therapies that would increase antitumor effects of treatment and reduce its side-effects. Materials and methods: Anticancer activity of oxicam derivatives (PR17 and PR18) alone and in combination with simvastatin on doxorubicin-resistant colon cancer cells was studied. Apoptosis was investigated via caspase-3 activation assay as well as via western blot analysis of expression of apoptotic components, B-cell lymphoma 2 protein (BCL2) and BCL2-associated X protein (BAX). Expression and activity of cyclo-oxygenase-2 (COX2) was also assessed. Results: Oxicam derivatives induced apoptosis through a caspase-3-dependent pathway, up-regulated BAX expression, and down-regulated BCL2 expression. Additionally, oxicam derivatives reduced expression and activity of COX2. Effect of oxicam derivatives on these processes was strongly potentiated by simvastatin. Conclusion: Oxicam derivatives at low concentrations effectively inhibit growth of cancer cells after co-administration with simvastatin. 

Retracted: No

PubPeer comments:
 I have a concern about Fig 3A. ![file] There is also a hint of a background discontinuity in the BAX band (requiring increased contrast to see clearly). ![file] ,
Metabolic response to selenium supplementation in women with polycystic ovary syndrome: a randomized, double-blind, placebo-controlled trial
Authors: Mehri Jamilian
Yasser Ghandi
Zohreh Fakhrie Kashan
Zatollah Asemi
Maryamalsadat Razavi
Tayebeh Bagherian
Journal: Clinical Endocrinology (2015)
Discipline: CLINICAL MEDICINE
Keywords: selenium supplementation; metabolic profiles; polycystic ovary syndrome; glucose homeostasis; lipid concentrations
Affiliations: Department of Gynecology and Obstetrics; School of Medicine; Arak University of Medical Sciences; Arak I.R. Iran, Department of Gynecology and Obstetrics; School of Medicine; Ardabil University of Medical Sciences; Ardabil I.R. Iran, Research Center for Biochemistry and Nutrition in Metabolic Diseases; Kashan University of Medical Sciences; Kashan I.R. Iran

Abstract:  Objective: We are aware of no study examining the effects of selenium supplementation on metabolic profiles of patients with polycystic ovary syndrome (PCOS). This study was conducted to evaluate the effects of selenium supplementation on glucose homeostasis parameters and lipid concentrations in women with PCOS. Design, patients and measurements: This randomized, double-blind, placebo-controlled trial was conducted among 70 women diagnosed with PCOS and aged 18-40 years old. Participants were randomly divided into two groups to receive 200 μg per day selenium supplements (N = 35) or placebo (N = 35) for 8 weeks. Fasting blood samples were taken at baseline and after 8 weeks intervention to quantify glucose, insulin and lipid concentrations. Results: After 8 weeks of intervention, subjects who received selenium supplements had significantly decreased serum insulin levels (-29·83 ± 47·29 vs +9·07 ± 77·12 pmol/l, P = 0·013), homeostasis model of assessment-insulin resistance (HOMA-IR) (-1·15 ± 1·81 vs +0·42 ± 3·09, P = 0·011), homeostatic model assessment-beta-cell function (HOMA-B) (-19·06 ± 30·95 vs +4·55 ± 47·99, P = 0·017) and increased quantitative insulin sensitivity check index (QUICKI) (+0·03 ± 0·04 vs +0·0009 ± 0·05, P = 0·032) compared with placebo. In addition, supplementation with selenium resulted in a significant reduction in serum triglycerides (-0·14 ± 0·55 vs +0·11 ± 0·30 mmol/l, P = 0·025) and VLDL-C concentrations (-0·03 ± 0·11 vs +0·02 ± 0·06 mmol/l, P = 0·025) compared with placebo. Conclusions: In conclusion, 200 microgram per day selenium supplementation for 8 weeks among PCOS women had beneficial effects on insulin metabolism parameters, triglycerides and VLDL-C levels; however, it did not affect FPG and other lipid profiles. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A36 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Morphine-induced delayed pre-conditioning against anoxia/reoxygenation injury in pulmonary artery endothelial cells: The role of mitochondrial KATP channels
Authors: Yueping Guo
Xiaoguang Cui
Wenzhi Li
Bing Zhang
Wengang Ding
Dongmei Li
Journal: Molecular Medicine Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Opioids; pre-conditioning; antiapoptotic effect; pulmonary artery endothelial cells; anoxia/reoxygenation injury
Affiliations: Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

Abstract:  Opioids produce delayed pre-conditioning (PC) in vivo and in vitro. Our previous research revealed that opioid‑induced delayed PC has an antiapoptotic effect on pulmonary artery endothelial cells (PAECs) suffering from anoxia/reoxygenation (A/R) injury. The present study hypothesized that activation of endothelial mitochondrial ATP‑sensitive potassium (KATP) channels may result in antiapoptotic effects and against dysfunction in PAECs. Cultured porcine PAECs underwent 16 h anoxia treatment, followed by 1 h reoxygenation, which occurred 24 h following pretreatment with saline (0.9% NaCl; w/v) or morphine (1 µM). To determine the underlying mechanism, a selective mitochondrial KATP inhibitor, 5‑hydroxydecanoic acid (5‑HD; 100 µM), and an opioid receptor antagonist, naloxone (Nal; 10 µM), were administered 30 min prior to the A/R load. The percentage of apoptotic cells was assessed by Annexin V‑fluorescein isothiocyanate staining, using a fluorescence‑activated cell sorter. The mRNA expression of intercellular cell adhesion molecule‑1 (ICAM‑1) was measured by reverse transcription‑quantitative polymerase chain reaction. The endothelin‑1 (ET‑1) content in the supernatant of PAECs cultures was estimated by radioimmunoassay. Compared with the control, A/R caused the apoptosis of PAECs, release of ET‑1 and increased mRNA expression of ICAM‑1. Morphine‑induced delayed PC significantly reduced PAEC apoptosis, increased the release of ET‑1 and reduced the mRNA expression of ICAM‑1 by ~1.7‑times, compared with A/R. The protective effect of morphine was abolished by pretreatment with 5‑HD and Nal, however, the two agents themselves failed to aggravate the A/R injury. These results suggested that morphine-induced delayed PC has a protective effect during A/R injury of PAECs. This effect may be mediated by mitochondrial KATP channels and is opioid receptor-dependent. 

Retracted: No

PubPeer comments:
 Figure 1A of this paper contains a number of flow cytometry plots most of which have repeated patterns of dots both vertically and horizontally in addition to a variety of other apparent anomalies. Can the authors explain how this might have occurred? ![file] ![file] ![file] ![file] ,
The plexin-A1 receptor activates vascular endothelial growth factor-receptor 2 and nuclear factor-kappaB to mediate survival and anchorage-independent growth of malignant mesothelioma cells
Authors: Alfonso Catalano
Antonio Procopio
Silvia Orciari
Raffaella Lazzarini
Silvia Di Nuzzo
Journal: Cancer Research (2009)
Discipline: CLINICAL MEDICINE
Keywords: Semaphorins; neuropilins; plexins; axonal guidance; tumor cells
Affiliations: Department of Molecular Pathology and Innovative Therapies, Marche University, Ancona, Italy. 

Abstract:  The semaphorins and their receptors, the neuropilins and the plexins, are constituents of a complex regulatory system that controls axonal guidance. Moreover, many types of tumor cells express various members of semaphorins and receptors, but the biological activities within tumor mass and the signal transduction mechanism(s) they use are largely unknown. Here, we show that in asbestos-related malignant pleural mesothelioma (MPM), Semaphorin-6D (Sema6D) and its receptor plexin-A1 are frequently expressed and trigger a prosurvival program that promotes anchorage-independent growth of MPM cells. Interestingly, the same response is also controlled by the tyrosine kinase receptors of vascular endothelial growth factor (VEGF) through a nuclear factor-kappaB (NF-kappaB)-dependent pathway. We found that in MPM cells, plexin-A1 and VEGF-receptor 2 (VEGF-R2) are associated in a complex. Moreover, the presence of Sema6D promotes the tyrosine phosphorylation of VEGF-R2 in a plexin-A1-dependent manner. This is necessary for basal and Sema6D-induced NF-kappaB transcriptional activity, and NF-kappaB mediates tumor cell survival. Expression of Sema6D and plexin-A1 is induced by asbestos fibers and overexpression of plexin-A1 in nonmalignant mesothelial cells inhibits cell death after asbestos exposure. This work identifies a new biological function of semaphorins in cancer cells and suggests the involvement of an undescribed survival pathway during MPM tumorigenesis. 

Retracted: No

PubPeer comments:
null, 
 Figure 6A. Much more similar than expected. https: imgur.com OS7c5uj , 
 #1 Figure 4B continued. Much more similar than expected. https: imgur.com JyHw3N1 ,
Toll-like receptors 2 and 4 mediate the capacity of mesenchymal stromal cells to support the proliferation and differentiation of CD34⁺ cells
Authors: Lailing Li
Xiucai Xu
Qiansong Cheng
Zimin Sun
Xingbing Wang
Jian Wang
Liang Xia
Journal: Experimental Cell Research (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bone marrow derived-mesenchymal stromal cells; BM-MSCs; toll-like receptors; TLRs; hematopoiesis
Affiliations: Department of Hematology of Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui, China. 

Abstract:  Bone marrow derived-mesenchymal stromal cells (BM-MSCs) are multipotent, nonhematopoietic progenitors in a hematopoietic microenvironment and indispensable for regulating hematopoiesis. Several studies have reported that toll-like receptors (TLRs) are expressed in mesenchymal stromal cells (MSCs) to modulate their biological functions. In this study, we investigated the possible role(s) of TLRs in mediating the hematopoiesis-supporting role of human BM-MSCs. Human BM-MSCs were analyzed for mRNA expression of TLR1-10 by reverse transcription-polymerase chain reaction. TLR1-6, but not TLR7-10 were expressed by BM-MSCs. The protein expression of TLR2 and TLR4 was also confirmed by flow cytometry. We further explored the role of TLR2 and TLR4 in mediating the capacity of BM-MSCs to support the proliferation and differentiation of CD34(+) hematopoietic stem/progenitor cells obtained from cord blood. BM-MSCs increased proliferation of CD34(+) cells and promoted the differentiation towards the myeloid lineage 7 or 14days after co-culture, as well as colony formation by those cells and the production of interleukin 1 (IL-1), IL-8, IL-11, stem cell factor (SCF), granulocyte colony-stimulating factor (CSF), macrophage CSF and granulocyte-macrophage CSF, if MSCs had been stimulated with TLR2 agonist (PAM(3)CSK(4)) or TLR4 agonist (LPS). Interestingly, although these effects were elevated in a different degree, a synergistic effect was not observed in BM-MSCs co-stimulated with PAM(3)CSK(4) and LPS. Together, our findings suggest that TLR2 and TLR4 signaling may indirectly regulate hematopoiesis by modulating BM-MSCs' functions. The increased hematopoietic proliferation and differentiation could be mediated, at least in part, by augmented hematopoiesis-related cytokine production of BM-MSCs. 

Retracted: No

PubPeer comments:
 Figure 1A * Red boxes: The CD31 and HLA-DR plots look remarkably similar ![file] ,
Downregulation of transcription factor TCTP elevates microRNA-200a expression to restrain Myt1L expression, thereby improving neurobehavior and oxidative stress injury in cerebral palsy rats
Authors: Zibo Liu
Yatao Pang
Xiaoxia He
Hongling Li
Wei Xu
Long Zhao
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MicroRNA-200a; Myt1l; Translationally controlled tumor protein; cerebral palsy; neurobehavior
Affiliations: The Second Department of Rehabilitation, The Second Hospital of Hebei Medical University, Shijiazhuang, China., The Department of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Abstract:  Transcription factors have already been proposed to work on some human diseases. Yet the role of translationally controlled tumor protein (TCTP) in cerebral palsy (CP) remains elusive. This study intends to examine the mechanism of TCTP on CP by regulating microRNA-200a (miR-200a).CP models of rats were established referring to the internationally recognized improved hypoxic ischemic encephalopathy modeling method. The neuroethology of rats, ultrastructure and pathological condition in brain tissues of rats were observed through several assays. The expression of TCTP, miR-200a, myelin transcription factor 1-like (Myt1L), tyrosine hydroxylase (TH) and inducible nitric oxide synthase (iNOS) along with apoptosis in brain tissues of rats was detected. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in brain tissues of rats were determined. The binding site between miR-200a and Myt1L was analyzed.TCTP and Myt1L were overexpressed and miR-200a was under-expressed in CP rats. Elevated miR-200a ameliorated neurobehavior of CP rats and pathological injury in brain tissues. Elevated miR-200a up-regulated TH, GSH, GSH-Px, and SOD levels, down-regulated iNOS, ROS, MDA, TNF-α, and IL-6 levels, and attenuated neuronal apoptosis in brain tissues of CP rats. Myt1L was a target gene of miR-200a.Altogether, our study suggested that diminution of transcription factor TCTP up-regulates miR-200a to limit Myt1L expression, thereby improving neurobehavior and oxidative stress injury in CP rats. 

Retracted: No

PubPeer comments:
 There is a numerical inconsistency for experiment 1. The paper reports n = 62 and degrees of freedom (df) = 62, even though df should be equal to n - 2. Out of curiosity, to investigate this further, I entered the numbers reported for the age variable into the SPRITE app . It shows that neither n = 62 nor n = 64 is consistent with the reported range (18-22), mean (18.91), and SD (1.04), assuming that age was recorded in whole years. ,
MicroRNA-1290 promotes esophageal squamous cell carcinoma cell proliferation and metastasis
Authors: Ri-Sheng Cao
Ming Li
Rui-Hua Shi
Xiao-Yan He
Li-Hua Ren
Ye Zhao
Shuo Li
Zhi-Mei Zhang
Yin-Lin Ji
Ya-Dong Feng
Journal: World journal of gastroenterology (2015)
Discipline: CLINICAL MEDICINE
Keywords: Esophageal squamous cell carcinoma; Invasion; Metastasis; MiR-1290; MicroRNA
Affiliations: Ming Li, Xiao-Yan He, Zhi-Mei Zhang, Shuo Li, Li-Hua Ren, Ri-Sheng Cao, Ya-Dong Feng, Yin-Lin Ji, Ye Zhao, Rui-Hua Shi, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China.

Abstract:  Aim: To investigate the biological role of miR-1290 in esophageal squamous cell carcinoma (ESCC) progression and invasion and the underlying mechanism. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate miR-1290 expression in ESCC tissue samples. The roles of miR-1290 in cell proliferation, migration and invasion were identified using miR-1290 mimic-transfected cells. In addition, the regulatory effect of miR-1290 on suppressor of cancer cell invasion (SCAI) was evaluated using qRT-PCR, Western blot analysis and a dual luciferase reporter assay. Results: miR-1290 was significantly upregulated in ESCC tissue samples compared with normal adjacent tissues (9.213 ± 1.150 vs 1.000 ± 0.0), (P &lt; 0.01). Upregulation of miR-1290 was associated with tumor differentiation (P = 0.021), N classification (P = 0.006) and tumor-node-metastasis stage (P = 0.021) in ESCC patients. Moreover, ectopic miR-1290 expression potently promoted ESCC cell growth (P &lt; 0.01), migration (P &lt; 0.01) and invasion (P &lt; 0.01) in vitro. miR-1290 overexpression in ESCC cell lines decreased SCAI expression at the translational level and reduced SCAI-driven luciferase-reporter activity (P &lt; 0.01). Conclusion: Our findings suggested that miR-1290 may play an oncogenic role in cellular processes of ESCC. 

Retracted: No

PubPeer comments:
 Figure 4 A and B use the same 4 images twice for different treatments. some of these images also appear to be used again in C and D (in one case flipped (orange box)). ![file] ,
Inï¿½vitro and inï¿½vivo anticancer effects of marmesin in U937 human leukemia cells are mediated via mitochondrial-mediated apoptosis, cell cycle arrest, and inhibition of cancer cell migration
Authors: Hong Li
Wen-Wei Xu
Lin Dong
Ke-Hong Bi
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Leukemia; anticancer agents; marmesin; cytotoxic effects; apoptosis
Affiliations: Department of Hematology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, Shandong 250014, P.R. China

Abstract:  Leukemia is one of the highly lethal cancers among all pediatric cancers. With limited drug options and the severe side effects associated with the current chemotherapy, there is pressing need to look for new and novel anticancer agents. Against this backdrop, in the present study we evaluated the anticancer activity of a natural coumarin, marmesin against human leukemia cell line U937 and normal human monocytes It was observed that marmesin exhibited an IC50 value of 40 µM and exerted its cytotoxic effects in a dose-dependent manner. However, the cytotoxic effects of marmesin were comparatively lower for the normal human monocytes as evident from the IC50 of 125 µM. Our results indicated that marmesin inhibits colony formation and induces apoptosis dose-dependently. We also investigated the effect of marmesin on the expression of Bax and Bcl-2 proteins. It was observed that marmesin treatment triggered upregulation of Bax and downregulation of Bcl-2 causing significant increase in the Bax/Bcl-2 ratio, marmesin could also induce ROS mediated alterations in mitochondrial membrane potential. Additionally, marmesin induced G2/M cell cycle arrest and significantly inhibited cell migration potential of leukemia cells at the IC50. Remarkably, marmesin prevent tumor growth significantly in vivo at the dosage of 30 mg/kg in vivo. These results strongly indicate that marmesin may prove to be a novel anticancer lead for the management of leukemia. 

Retracted: Yes

PubPeer comments:
 Figure 6.  Impacts of morphine pretreatment on TLR4 and p65 in rat heart tissues . Panels for TLR4 and p65 (morphine-pretreated group) overlap, and are unlikely to have come from different immunohistochemistry stains. ![file] ,
TARBP2 negatively regulates IFN-β production and innate antiviral response by targeting MAVS
Authors: Ting Ling
Liang-Guo Xu
Weiying Wang
Hua Rao
Changsheng Li
Sheng-Na Li
Lingzhen Cao
Guang-Xiu Weng
Hong-Bing Shu
Journal: Molecular Immunology (2018)
Discipline: IMMUNOLOGY
Keywords: IFN-Β; MAVS; RIG-I; TARBP2; TRAF3.
Affiliations: Key Laboratory of Functional Small Organic Molecules, Ministry of Education and College of Life Science, Jiangxi Normal University, Nanchang, Jiangxi, 330022, China., Medical Research Institute, School of Medicine, Wuhan University, Wuhan, 430071, China. Electronic address: ., Key Laboratory of Functional Small Organic Molecules, Ministry of Education and College of Life Science, Jiangxi Normal University, Nanchang, Jiangxi, 330022, China. Electronic address: .

Abstract:  MAVS as an essential receptor protein for anti-virus innate immunity plays an important role in the production of virus-induced typeⅠ interferon and regulation of interferon regulatory factor 3/7. Understanding the MAVS-mediated antiviral signaling pathway can provide detailed insights. In this study, we identify transactivation response element RNA-binding protein (TARBP2), as an inhibitor of the cellular protein kinase PKR, negatively regulates virus -induced IFN-β production by targets MAVS. Overexpression of TARBP2 inhibits virus-induced IFN-β production as well as cellular antiviral response. Then knockdown of TARBP2 inhibited virus-induced IFN-β signaling. Further studies demonstrated that TARBP2 interacted with MAVS and targeted MAVS to abrogate MAVS-RIG-I and MAVS-TRAF3 association. Our findings suggest that TARBP2 is an important non-redundant virus-mediated negative regulator of typeⅠ interferon. 

Retracted: No

PubPeer comments:
 Actin immunoblotting images reappeared in Fig.5D. ![file] , 
 #1 I note an incongruity with the green arrow. Would you consider this a concern? *** ![file] , 
 #1 Dr. Liang-Guo Xu is responsible for this paper and will address your comments. , 
 I am the first author.Thank you very much for pointing out the mistakes of Fig. 5D. We have carefully examined our raw data. It turned out that we had inadvertently used images analyzed from theu00a0TRAF3-K63 group to represent theu00a0TRAF3-K48group in Fig. 3C during the figure preparation. The authors apologize for the mistakes. This error doesn t affect the results or conclusions of the figure. We haveu00a0contacted the journal and request for a correction. , 
 #4 Thank you for your reply. Could the authors please post the original uncropped scans here? , 
 The following is a comparison between the original picture and the figure (red box). Due to the improper experiment process, a duplicate sample was added, so one of the lanes was cut off, and the picture itself was not modified. , 
 ![file] , 
 #7 Thank you again. While the splice might be more clearly identified for readers in the paper, Iu2019m also puzzled why this splice does not also appear in the bands in the lower portion of this figure. Apologies, but I am confused. ,
Long noncoding RNA PROX1-AS1 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6
Authors: J-F Li
L Zhao
X-J Tong
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; PROX1-AS1; ovarian cancer; metastasis; proliferation
Affiliations: Department of Gynecology Center, The First Affiliated Hospital of XinJiang Medical University, Urumqi, China. .

Abstract:  Objective: Recently, the role of long noncoding RNAs (lncRNAs) in tumor progression has attracted much attention worldwide. Numerous studies have identified lncRNA PROX1-AS1 as an oncogene in cancers. Therefore, the aim of this research was to explore the function of PROX1-AS1 in the development of ovarian cancer. Patients and methods: PROX1-AS1 expression in both ovarian cancer patients and normal subjects was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Subsequently, PROX1-AS1 shRNA was constructed and transfected in vitro. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, colony formation assay, transwell assay, and Matrigel assay were utilized to detect the function of PROX1-AS1 in ovarian cancer. In addition, the potential mechanism was explored using qRT-PCR and Western blot assay. Results: PROX1-AS1 was highly expressed in ovarian carcinoma samples and cell lines (p&lt;0.05). The proliferation, migration, and invasion of ovarian cells were significantly inhibited after PROX1-AS1 was downregulated in vitro (p&lt;0.05). Besides, the mRNA and protein expressions of KLF6 were significantly promoted after PROX1-AS1 knockdown in ovarian cancer cells (p&lt;0.05). Further functional assays showed that KLF6 expression was negatively correlated with PROX1-AS1 expression in ovarian cancer samples. Conclusions: PROX1-AS1 enhances the metastasis and proliferation of ovarian cancer cells via suppressing KLF6. Our findings suggest that PROX1-AS1 may be applied as a novel target for therapy of ovarian cancer. 

Retracted: Yes

PubPeer comments:
 Figure 4A. Much more similar than you would expect. https: imgur.com NXftGQf , 
 Figures 5A and 6B. Much more similar than you would expect even though the experimental conditions are different. https: imgur.com tsCeBzu ,
CRABP2 promotes myoblast differentiation and is modulated by the transcription factors MyoD and Sp1 in C2C12 cells
Authors: Kui Li
Zhonglin Tang
Shulin Yang
Jing Yuan
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: CRABP2; myogenesis; myogenic transformation; cell cycle regulation; core promoter
Affiliations: State Key Laboratory for Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, People's Republic of China.

Abstract:  Cellular retinoic acid binding protein 2 (CRABP2), a member of a family of specific carrier proteins for Vitamin A, belongs to a family of small cytosolic lipid binding proteins. Our previous study suggested that CRABP2 was involved in skeletal muscle development; however, the molecular function and regulatory mechanism of CRABP2 in myogenesis remained unclear. In this study, we found that the expression of the CRABP2 gene was upregulated during C2C12 differentiation. An over-expression assay revealed that CRABP2 promotes myogenic transformation by regulating the cell cycle during C2C12 differentiation. The region from -459 to -4 bp was identified as the core promoter and contains a TATA box, a GC box and binding sites for the transcription factors MyoD and Sp1. Over-expression, site-directed mutagenesis and EMSA assays indicated that the transcription factors MyoD and Sp1 regulate CRABP2 expression and promote myoblast differentiation in C2C12 cells. 

Retracted: No

PubPeer comments:
 Figure 1 * Orange boxes: The CRABP1 and CRBP2 panels appear to look similar to each other. Note the position of two small light specks, in an enhanced-contrast image (shown with yellow arrows). ![file] ,
MicroRNA-125b promotes neurons cell apoptosis and Tau phosphorylation in Alzheimer's disease
Authors: Xiaohui Ma
Linlin Liu
Jing Meng
Journal: Neuroscience letters (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer’s disease; Forkhead box Q1; MicroRNA-125b; Neurons cell apoptosis; Tau phosphorylation.
Affiliations: Department of Geriatrics, Xi'an No. 1 Hospital, Xi'an 710002, China., Open Ward, Qingdao Mental Health Center, Qingdao 266034, China., Department of Geriatrics, Wuhan Mental Health Center, No. 93, Youyi Road, Qiaokou District, Wuhan 430022, China. Electronic address: .

Abstract:  Alzheimer's disease (AD) is considered as one of the most common neural degenerative diseases in human. Although the continuous investigations about AD have been made in recent decades, the pathogenesis of this disease is still not definitely confirmed. MicroRNA-125b (miR-125b) is extensive expressed in many types of human tissues and played pivotal regulatory roles in diverse biological process. In the present study, we aimed to explore the roles of miR-125b in regulating neurons cell apoptosis under AD condition. The possible molecular mechanisms were also investigated. We found that miR-125b was up-regulated in patients with AD. Transfection with miR-125b significantly enhanced the apoptosis of neurons cells and phosphorylation of Tau by activation of cyclin-dependent kinase 5 (CDK5) and p35/25. Forkhead box Q1 (FOXQ1) was the direct target gene of miR-125b, which involved in the effects of miR-125b on neurons cell apoptosis and phosphorylation of Tau. Our research interpreted the mechanism of up-regulation of miR-125b in pathological Tau phosphorylation and AD occurrence. miR-125b may be a novel regulator of AD progress and could be as a therapeutic target for AD therapy. 

Retracted: No

PubPeer comments:
 Figure 2. * Boxes of the same color highlight panels or parts of panels that look remarkably similar ![file] , 
 Figure 3. * Boxes of the same color highlight panels or parts of panels that look remarkably similar, also to the Figure 2 panels ![file] ,
Analytic thinking promotes religious disbelief
Authors: Ara Norenzayan
Will M Gervais
Journal: Science (2012)
Discipline: Multidisciplinary
Keywords: cognitive underpinnings; religious belief; experimental research; cognitive processes; analytic processing
Affiliations: University of British Columbia, Vancouver, BC, Canada. 

Abstract:  Scientific interest in the cognitive underpinnings of religious belief has grown in recent years. However, to date, little experimental research has focused on the cognitive processes that may promote religious disbelief. The present studies apply a dual-process model of cognitive processing to this problem, testing the hypothesis that analytic processing promotes religious disbelief. Individual differences in the tendency to analytically override initially flawed intuitions in reasoning were associated with increased religious disbelief. Four additional experiments provided evidence of causation, as subtle manipulations known to trigger analytic processing also encouraged religious disbelief. Combined, these studies indicate that analytic processing is one factor (presumably among several) that promotes religious disbelief. Although these findings do not speak directly to conversations about the inherent rationality, value, or truth of religious beliefs, they illuminate one cognitive factor that may influence such discussions. 

Retracted: No

PubPeer comments:
 ![file] In Table 1, the case number marked by yellow of all three groups is 262!!! ,
Glycogen synthase kinase-3beta induces neuronal cell death via direct phosphorylation of mixed lineage kinase 3
Authors: Rajakishore Mishra
James R Woodgett
Manoj K Barthwal
Ajay Rana
Malay Chatterjee
Lucas Wong
Basabi Rana
Gautam Sondarva
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MLK3; GSK-3beta; JNK pathway; neurodegenerative diseases; NGF withdrawal
Affiliations: Department of Internal Medicine, Cardiovascular and Cancer Research Institute, The Texas A & M University System-HSC, College of Medicine, Texas 76504, USA.

Abstract:  Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase member that activates the c-Jun N-terminal kinase (JNK) pathway. Aberrant activation of MLK3 has been implicated in neurodegenerative diseases. Similarly, glycogen synthase kinase (GSK)-3beta has also been shown to activate JNK and contribute to neuronal apoptosis. Here, we show a functional interaction between MLK3 and GSK-3beta during nerve growth factor (NGF) withdrawal-induced cell death in PC-12 cells. The protein kinase activities of GSK-3beta, MLK3, and JNK were increased upon NGF withdrawal, which paralleled increased cell death in NGF-deprived PC-12 cells. NGF withdrawal-induced cell death and MLK3 activation were blocked by a GSK-3beta-selective inhibitor, kenpaullone. However, the MLK family inhibitor, CEP-11004, although preventing PC-12 cell death, failed to inhibit GSK-3beta activation, indicating that induction of GSK-3beta lies upstream of MLK3. In GSK-3beta-deficient murine embryonic fibroblasts, ultraviolet light was unable to activate MLK3 kinase activity, a defect that was restored upon ectopic expression of GSK-3beta. The activation of MLK3 by GSK-3beta occurred via phosphorylation of MLK3 on two amino acid residues, Ser(789) and Ser(793), that are located within the C-terminal regulatory domain of MLK3. Furthermore, the cell death induced by GSK-3beta was mediated by MLK3 in a manner dependent on its phosphorylation of the specific residues within the C-terminal domain by GSK-3beta. Taken together, our data provide a direct link between GSK-3beta and MLK3 activation in a neuronal cell death pathway and identify MLK3 as a direct downstream target of GSK-3beta. Inhibition of GSK-3 is thus a potential therapeutic strategy for neurodegenerative diseases caused by trophic factor deprivation. 

Retracted: No

PubPeer comments:
null, 
null, 
 #1 I agree that these are more likely than not to be the same. Do the authors have access to the original scans? *** ![file] *** Inverse ![file] *** False color ![file] ,
Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis
Authors: Shyam Biswal
Siddhartha Srivastava
Christine Happel
Wyeth W Wasserman
Deepti Malhotra
Anju Singh
David Arenillas
Elodie Portales-Casamar
Thomas W Kensler
Casper Shyr
Nobunao Wakabayashi
Journal: Nucleic Acids Research (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Nrf2; transcription factor; oxidative stress; electrophilic stress; Keap1
Affiliations: Department of Environmental Health Sciences Department, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.

Abstract:  The Nrf2 (nuclear factor E2 p45-related factor 2) transcription factor responds to diverse oxidative and electrophilic environmental stresses by circumventing repression by Keap1, translocating to the nucleus, and activating cytoprotective genes. Nrf2 responses provide protection against chemical carcinogenesis, chronic inflammation, neurodegeneration, emphysema, asthma and sepsis in murine models. Nrf2 regulates the expression of a plethora of genes that detoxify oxidants and electrophiles and repair or remove damaged macromolecules, such as through proteasomal processing. However, many direct targets of Nrf2 remain undefined. Here, mouse embryonic fibroblasts (MEF) with either constitutive nuclear accumulation (Keap1(-/-)) or depletion (Nrf2(-/-)) of Nrf2 were utilized to perform chromatin-immunoprecipitation with parallel sequencing (ChIP-Seq) and global transcription profiling. This unique Nrf2 ChIP-Seq dataset is highly enriched for Nrf2-binding motifs. Integrating ChIP-Seq and microarray analyses, we identified 645 basal and 654 inducible direct targets of Nrf2, with 244 genes at the intersection. Modulated pathways in stress response and cell proliferation distinguish the inducible and basal programs. Results were confirmed in an in vivo stress model of cigarette smoke-exposed mice. This study reveals global circuitry of the Nrf2 stress response emphasizing Nrf2 as a central node in cell survival response. 

Retracted: No

PubPeer comments:
 In Figure 5A, several discontinuities are seen, indicating that the data have been modified. ![file] The research group has a dubious prehistory: https: ori.hhs.gov content case-summary-malhotra-deepti ,
Metastable macromolecular complexes containing high mobility group nucleosome-binding chromosomal proteins in HeLa nuclei
Authors: Vasily V Ogryzko
Yuri V Postnikov
Jae-Hwan Lim
Michael Bustin
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: HMGN proteins; nucleosomes; chromatin structure; macromolecular complexes; nuclear activities
Affiliations: Protein Section, CCR, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA.

Abstract:  High mobility group nucleosome-binding (HMGN) proteins belong to a family of nuclear proteins that bind to nucleosomes and enhance transcription from chromatin templates by altering the structure of the chromatin fiber. The intranuclear organization of these proteins is dynamic and related to the metabolic state of the cell. Here we report that approximately 50% of the HMGN proteins are organized into macromolecular complexes in a fashion that is similar to that of other nuclear activities that modify the structure of the chromatin fiber. We identify several distinct HMGN-containing complexes that are relatively unstable and find that the inclusion of HMGN in the complexes varies according to the metabolic state of the cell. The nucleosome binding ability of HMGN in the complex is stronger than that of the free HMGN. We suggest that the inclusion of HMGN proteins into metastable multiprotein complexes serves to target the HMGN proteins to specific sites in chromatin and enhances their interaction with nucleosomes. 

Retracted: No

PubPeer comments:
 ***There are similar Western bolt bands (red rectangles) in FIG.2B and FIG. 2D.** * ![file] ,
The relationship between CD40 gene polymorphism and unstable coronary atherosclerotic plaques
Authors: Cuiping Wang
Jinchuan Yan
Ping Yang
Guanghua Chen
Rongzeng Du
Journal: Clinical Cardiology (2010)
Discipline: CLINICAL MEDICINE
Keywords: CD40 polymorphism; acute coronary syndromes; vulnerable plaque; rupture risk; coronary angiography
Affiliations: Division of Cardiology, Department of Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China.

Abstract:  Background: Recently, CD40 polymorphism was found to be associated with acute coronary syndromes. However, few study was involved in the relationship between CD40 polymorphism and the risk of the vulnerable plaque to rupture so far. Materials and methods: A total of 699 patients who have received coronary angiography were divided into 3 groups according to the morphological division of the plaques: complex lesions (343 cases), smooth lesions (131 cases), and control group (225 cases).The gene polymorphism was measured by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) and identified by sequencing. Results: The CC genotype and C allele frequency of the CD40 gene in the complex lesions group is significantly higher than in the smooth lesions group and the control group (P &lt; .001), while the TT genotype frequency in the complex lesions group is significantly lower than that of the smooth lesions group and the control group (P &lt; .001). The C allele increased disruption risk of the plaques in the complex lesions group as compared with the smooth lesions group (odds ratio [OR]: 1.697, 95% confidence interval [CI]: 1.273-2.261). No significant differences in genotypes or allele frequencies were found between the smooth lesions group and the control group. Conclusion: Our results suggested that CD40 (-1C/T) polymorphism was associated with unstable coronary atherosclerotic plaques. The C allele frequency increased the risk of disruption of the coronary atherosclerotic plaques. 

Retracted: No

PubPeer comments:
 Figure 3. Several panels appear to show an overlap, suggesting that fewer individual specimens are visible than expected. Boxes of the same color show areas that look similar. ![file] ,