PReD-Bench/PRed-Bench huggingface dataset:
Association between mean platelet volume and major adverse cardiac events in percutaneous coronary interventions: a systematic review and meta-analysis
Authors: Chen Li
Nan Li
Sen He
Zhongxiu Chen
Yong He
Xiaorong Zhou
Jing Wang
Journal: Coronary artery disease (2020)
Discipline: CLINICAL MEDICINE
Keywords: Platelets; Mean platelet volume (MPV); Percutaneous coronary interventions (PCI); Major adverse cardiac event (MACE); Meta-analysis
Affiliations: Department of Cardiology, West China Hospital of Sichuan University., Information Center of West China Hospital of Sichuan University., West China School of Pharmacy Sichuan University., Department of Nursing, Community Health Center of Shuangnan Wuhou District, Chengdu, China.

Abstract:  Platelets with high hemostatic activity play a key role during percutaneous coronary interventions (PCI), and in recent years, mean platelet volume (MPV) has been looked upon as a crucial indicator of platelet reactivity. Thus, MPV may emerge as a potential gauge for the measurement of major adverse cardiac event (MACE) risks in PCI patients. This study aimed to conduct a meta-analysis illustrating the association between MPV and long-term MACE in PCI. The Cochrane Library, Pubmed, EMBASE, Ovid MEDLINE, and BIOSIS databases were used to search for relevant studies from their inception to 30 June 2019. All studies reporting incidences of MACE and MPV in PCI patients were retained. Data extraction was performed by three independent reviewers. A total of 33 studies were included in this meta-analysis. The results indicated that patients with MACE had a significantly larger MPV than those without, with an unstandardized mean difference (USMD) of 0.29 fL (95% CI, 0.04-0.54). The USMD of MPV in deceased patients was 0.39 fL (95% CI, 0.09-0.68). The results also indicated that patients with larger MPV were at greater risks of having MACE and higher incidence of mortality than those with smaller MPV, with a pooled risk ratio of 1.81 (95% CI, 1.29-2.55) and 2.34 (95% CI, 1.52-3.60), respectively. These findings indicate a significant association between larger MPV and MACE in PCI patients. Consequently, MPV, an easily accessible indicator, might be helpful in PCI patients' risk assessment and stratification. 

Retracted: No

PubPeer comments:
 The reference list is attached. Out of the total 50 papers cited, 25 are authored by G.W. Wei and his co-authors.     , 
 This paper is essentially same with the following paper in the same volume of the same journal Chang-Quan Zhang and Qun Zou. Model for evaluating the performance of vehicular Ad Hoc network with triangular fuzzy information. International Journal of Knowledge-based and Intelligent Engineering Systems 21 (2017) 181u2013187. DOI 10.3233 KES-170362 https: pubpeer.com publications 95CC51501C6E5DE068571DB325824B See also a 2019 paper on https: pubpeer.com publications 84600E170AB9E4925C7763FA9BCC40#1    ,
Black ginseng-enriched Chong-Myung-Tang extracts improve spatial learning behavior in rats and elicit anti-inflammatory effects in¬†vitro
Authors: Evelyn Saba
Hyun-Kyoung Kim
Man-Hee Rhee
Sung-Dae Kim
Seong-Soo Roh
Da-Hye Jeong
Seung-Hyung Kim
Journal: Journal of Ginseng Research (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: BV2 cells; anti-inflammation; black ginseng; cytokines; learning.
Affiliations: Laboratory of Physiology and Cell Signaling, College of Veterinary Medicine, Kyungpook National University, Daegu, Korea., College of Korean Medicine, Daegu Haany University, Daegu, Korea., Institute of Traditional Medicine and Bioscience, Daejeon University, Daejeon, Korea., Department of Food Science and Engineering, Seowon University, Chungbuk, Korea.

Abstract:  Background: Chong-Myung-Tang (CMT) extract is widely used in Korea as a traditional herbal tonic for increasing memory capacity in high-school students and also for numerous body ailments since centuries. The use of CMT to improve the learning capacity has been attributed to various plant constituents, especially black ginseng, in it. Therefore, in this study, we have first investigated whether black ginseng-enriched CMT extracts affected spatial learning using the Morris water maze (MWM) test. Their molecular mechanism of action underlying improvement of learning and memory was examined in vitro. Methods: We used two types of black ginseng-enriched CMT extracts, designated as CM-1 and CM-2, and evaluated their efficacy in the MWM test for spatial learning behavior and their anti-inflammatory effects in BV2 microglial cells. Results: Our results show that both black ginseng-enriched CMT extracts improved the learning behavior in scopolamine-induced impairment in the water maze test. Moreover, these extracts also inhibited nitric oxide production in BV2 cells, with significant suppression of expression of proinflammatory cytokines, especially inducible nitric oxide synthase, cyclooxygenase-2, and interleukin-1Œ≤. The protein expression of mitogen-activated protein kinase and nuclear factor-Œ∫B pathway factors was also diminished by black ginseng-enriched CMT extracts, indicating that it not only improves the memory impairment, but also acts a potent anti-inflammatory agent for neuroinflammatory diseases. Conclusion: Our research for the first time provides the scientific evidence that consumption of black ginseng-enriched CMT extract as a brain tonic improves memory impairment. Thus, our study results can be taken as a reference for future neurobehavioral studies. 

Retracted: No

PubPeer comments:
 Some odd use of blot data here:  Can the authors explain? ,
Reduction of transforming growth factor-Œ≤1 expression in leukemia and its possible role in leukemia development
Authors: Hui-Fang Huang
Yong Wu
Mei-Juan Huang
Yuan-Zhong Chen
Ping Chen
Journal: Leukemia & lymphoma (2012)
Discipline: CLINICAL MEDICINE
Keywords: transforming growth factor-Œ≤1; leukemia development; TGF-Œ≤1 levels; cell apoptosis; G1 phase
Affiliations: Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou, China.

Abstract:  The expression of transforming growth factor-Œ≤1 (TGF-Œ≤1) in leukemic cells and sera from patients with leukemia and its possible role in leukemia development were studied. TGF-Œ≤1 levels in culture supernatants from leukemic cells were significantly lower than those from normal bone marrow mononuclear cells. Serum TGF-Œ≤1 levels in leukemic patients were significantly lower compared with healthy controls, but returned to normal in patients achieving complete remission, and decreased when patients relapsed. TGF-Œ≤1 mRNA expression levels were significantly higher in normal bone marrow mononuclear cells but lower in leukemic cells compared with normal CD34 + cells. After transfection of the TGF-Œ≤1 gene to HL-60 cells, cell apoptosis was detected. Moreover, by flow cytometry analysis, cells arrested in G1 phase were 62% for TGF-Œ≤1 transfected cells and 44% for controls. Transfection of exogenous TGF-Œ≤1 gene inhibited HL60 cells xenograft growth in nude mice, and prolonged survival of tumor-bearing mice compared with the controls. Decreased endogenous TGF-Œ≤1 expression in leukemia cells may be involved in leukemia development, Transfection of exogenous TGF-B1 gene to HL60 can inhibit the proliferation of the cells and induce cell apoptosis by down regulating bcl-2, hTERT (human telomerase reverse transcriptase) and c-myc expression. 

Retracted: No

PubPeer comments:
 Figure 4B. Some of these mice have very large tumors. It is hard to see where the mouse ends and the tumor begins. Could the authors please comment on this? Where the tumors in accordance with international guidelines on animal ethics?  ,
Modeling Brain Somatic Mosaicism With Cerebral Organoids, Including a Note on Mutant Microglia
Authors: Bert M Verheijen
Journal: Frontiers in Molecular Neuroscience (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 3D organoids; brain genomic mosaicism; cell models; induced pluripotent stem cells; neural circuits
Affiliations: Department of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands., Department of Neurology and Neurosurgery, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.

Abstract:  The brain is a genomic mosaic. Cell-to-cell genomic differences, which are the result of somatic mutations during development and aging, contribute to cellular diversity in the nervous system. This genomic diversity has important implications for nervous system development, function, and disease. Brain somatic mosaicism might contribute to individualized behavioral phenotypes and has been associated with several neuropsychiatric and neurodegenerative disorders. Therefore, understanding the causes and consequences of somatic mosaicism in neural circuits is of great interest. Recent advances in 3D cell culture technology have provided new means to study human organ development and various human pathologies in vitro. Cerebral organoids ("mini-brains") are pluripotent stem cell-derived 3D culture systems that recapitulate, to some extent, the developmental processes and organization of the developing human brain. Here, I discuss the application of these neural organoids for modeling brain somatic mosaicism in a lab dish. Special emphasis is given to the potential role of microglial mutations in the pathogenesis of neurodegenerative diseases. 

Retracted: Yes

PubPeer comments:
 The journal retracts the 14 November 2019 article cited above. Following publication, it was brought to our attention that the author used and published primary research data, which was generated together with other researchers in the laboratory, without permission and without a mention to the other contributors. In particular, the human iPSCs data included does not have permission from the authorities or the patients. Unauthorized data use is a breach of Frontiers guidelines and those of the Committee on Publication Ethics. As such, this article is being retracted. The author does not concur with the retraction and sincerely regret any inconvenience this may have caused to the reviewers, editors, and readers of Frontiers in Molecular Neuroscience. https: www.frontiersin.org articles 10.3389 fnmol.2020.628401 full ,
Zyflamend induces apoptosis in pancreatic cancer cells via modulation of the JNK pathway
Authors: Ahmed Bettaieb
Mohammed Alquraishi
Dina Alani
Brynn Voy
Dexter L Puckett
Dallas Donohoe
Samah Chahed
Jay Whelan
Journal: Cell Communication and Signaling (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Autophagy; ER stress; JNK; Pancreatic neuroendocrine tumor cells
Affiliations: Department of Nutrition, University of Tennessee Knoxville, 1215 Cumberland Avenue, 229 Jessie Harris Building, Knoxville, TN, 37996-0840, USA., Tennessee Agricultural Experiment Station, University of Tennessee Institute of Agriculture, Knoxville, TN, 37996-0840, USA., Graduate School of Genome Science and Technology, University of Tennessee, Knoxville, TN, 37996-0840, USA., Department of Nutrition, University of Tennessee Knoxville, 1215 Cumberland Avenue, 229 Jessie Harris Building, Knoxville, TN, 37996-0840, USA. ., Graduate School of Genome Science and Technology, University of Tennessee, Knoxville, TN, 37996-0840, USA. ., Department of Biochemistry, Cellular and Molecular Biology, University of Tennessee, Knoxville, TN, 37996-0840, USA. .

Abstract:  Background: Current pharmacological therapies and treatments targeting pancreatic neuroendocrine tumors (PNETs) have proven ineffective, far too often. Therefore, there is an urgent need for alternative therapeutic approaches. Zyflamend, a combination of anti-inflammatory herbal extracts, that has proven to be effective in various in vitro and in vivo cancer platforms, shows promise. However, its effects on pancreatic cancer, in particular, remain largely unexplored. Methods: In the current study, we investigated the effects of Zyflamend on the survival of beta-TC-6 pancreatic insulinoma cells (Œ≤-TC6) and conducted a detailed analysis of the underlying molecular mechanisms. Results: Herein, we demonstrate that Zyflamend treatment decreased cell proliferation in a dose-dependent manner, concomitant with increased apoptotic cell death and cell cycle arrest at the G2/M phase. At the molecular level, treatment with Zyflamend led to the induction of ER stress, autophagy, and the activation of c-Jun N-terminal kinase (JNK) pathway. Notably, pharmacological inhibition of JNK abrogated the pro-apoptotic effects of Zyflamend. Furthermore, Zyflamend exacerbated the effects of streptozotocin and adriamycin-induced ER stress, autophagy, and apoptosis. Conclusion: The current study identifies Zyflamend as a potential novel adjuvant in the treatment of pancreatic cancer via modulation of the JNK pathway. Video abstract. 

Retracted: No

PubPeer comments:
 Concern about Figures 1F, 2A, 2E, and 5F. * Boxes of the same color show areas identified by ImageTwin as highly similar. Some of these might be showing the same experiments (the yellow and pink boxes perhaps), but most others seem to display different experiments.  This work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (R00DK100736) to A.B. ,
Downregulation of microRNA-30d promotes cell proliferation and invasion by targeting LRH-1 in colorectal carcinoma
Authors: Likun Yan
Jian Qiu
Jianfeng Yao
Journal: International Journal of Molecular Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: miR-30d; colorectal cancer; tumor suppressor; LRH-1; Wnt/Œ≤-catenin signaling
Affiliations: Department of General Surgery, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.

Abstract:  The aberrant expression of miR-30d has been reported in several types of human malignancies. However, its biological function in colorectal cancer (CRC) remains largely unknown. In this study, we identified that miR‚Ä?0d was significantly downregulated in CRC tissues compared to that observed in normal controls as detected by RT‚ÄëqPCR analysis. Downregulation of miR‚Ä?0d was significantly associated with aggressive clinicopathological parameters including tumor differentiation, invasive depth, TNM stage, lymph node metastasis, distant metastasis, and poor prognosis. Furthermore, functional analysis revealed that overexpression of miR‚Ä?0d significantly inhibited cell proliferation, caused cell cycle arrest at the G0/G1 phase, suppressed cell migration and invasion, induced cell apoptosis in vitro, and decreased tumor growth in a xenograft mouse model. Bioinformatic analysis and dual‚Äëluciferase reporter assay revealed that liver receptor homologue‚Ä? (LRH‚Ä?) is a direct target of miR‚Ä?0d in CRC cells. Rescue assay showed that LRH‚Ä? overexpression could restore the inhibitory effect of miR‚Ä?0d on CRC cells. In addition, miR‚Ä?0d overexpression suppressed the activation of key components of the Wnt/Œ≤‚Äëcatenin signaling pathway, Œ≤‚Äëcatenin, c‚ÄëMyc and cyclin D1, which contributed to the inhibition of CRC development. Thus, our findings suggest that miR‚Ä?0d functions as a tumor suppressor against CRC development and miR‚Ä?0d/LRH‚Ä?/Wnt signaling may be novel potential targets for CRC treatment. 

Retracted: No

PubPeer comments:
 Fig 4B.  cell apoptosis of LoVo and SW480 cell lines with miR-30d mimics or miR-NC transfection were analyzed by flow cytometry. In the four left-hand panels, there are no cells points in the upper quadrants, but instead a misty haze hovers there - more visible with enhanced contrast (see the version at right).  Can the authors speculate on the source of this misty haze, and why it is so similar in the LoVo Control and LoVo NC panels - almost like a half-erased version of the upper quadrants in the LoVo-miR-30d panel? Also similar in the SW480 Control and SW480 NC panels, almost like a half-erased version of the upper quadrants in the SW480-miR-30d panel? Zooming a little.  ,
Modulation of Acid-sensing Ion Channel 1a by Intracellular pH and Its Role in Ischemic Stroke
Authors: Ming-Hua Li
Roger P Simon
Xue-Chao Feng
Tao Yang
Zhi-Gang Xiong
Tian-Dong Leng
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: acid sensing ion channel (ASIC); brain; electrophysiology; ischemia; patch clamp.
Affiliations: From the Department of Neurological Surgery, Oregon Health and Science University, Portland, Oregon 97239, ., the Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, Georgia 30310, and., the Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Cytology and Genetics, Northeast Normal University, 130000 Changchun, China., the Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, Georgia 30310, and .

Abstract:  An important contributor to brain ischemia is known to be extracellular acidosis, which activates acid-sensing ion channels (ASICs), a family of proton-gated sodium channels. Lines of evidence suggest that targeting ASICs may lead to novel therapeutic strategies for stroke. Investigations of the role of ASICs in ischemic brain injury have naturally focused on the role of extracellular pH in ASIC activation. By contrast, intracellular pH (pHi) has received little attention. This is a significant gap in our understanding because the ASIC response to extracellular pH is modulated by pHi, and activation of ASICs by extracellular protons is paradoxically enhanced by intracellular alkalosis. Our previous studies show that acidosis-induced cell injury in in vitro models is attenuated by intracellular acidification. However, whether pHi affects ischemic brain injury in vivo is completely unknown. Furthermore, whereas ASICs in native neurons are composed of different subunits characterized by distinct electrophysiological/pharmacological properties, the subunit-dependent modulation of ASIC activity by pHi has not been investigated. Using a combination of in vitro and in vivo ischemic brain injury models, electrophysiological, biochemical, and molecular biological approaches, we show that the intracellular alkalizing agent quinine potentiates, whereas the intracellular acidifying agent propionate inhibits, oxygen-glucose deprivation-induced cell injury in vitro and brain ischemia-induced infarct volume in vivo Moreover, we find that the potentiation of ASICs by quinine depends on the presence of the ASIC1a, ASIC2a subunits, but not ASIC1b, ASIC3 subunits. Furthermore, we have determined the amino acids in ASIC1a that are involved in the modulation of ASICs by pHi. 

Retracted: No

PubPeer comments:
 Figure 2A, two of the slices in the aCSF and quinine condition look very similar.  ,
Suppression of BMX‚ÄêARHGAP fusion gene inhibits epithelial‚Äêmesenchymal transition in gastric cancer cells via RhoA‚Äêmediated blockade of JAK/STAT axis
Authors: Yong Ji
Jian-Jiang Wang
Li Ding
Xiao-Feng Xu
Feng Gao
Jin-Song Ye
Lan Tao
Li-Juan Huang
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: JAK/STAT axis; RhoA; bone marrow X kinase Rho GTPase activating protein 12 (BMX-ARHGAP) fusion gene; epithelial-mesenchymal transition (EMT); gastric cancer (GC).
Affiliations: Department of Clinical Laboratory Jingjiang People's Hospital Jingjiang China, Department of Gastrointestinal Surgery Jingjiang People‚Äôs Hospital Jingjiang China

Abstract:  Gastric cancer (GC) is one of the main causes of cancer-related mortality worldwide. Epithelial-mesenchymal transition (EMT) is an important biological process involving the process by which malignant tumor cells obtain the ability of migration, invasion, resistance of apoptosis, and degradation in the extracellular matrix. The current study aimed at investigating whether bone marrow X kinase Rho GTPase activating protein 12 (BMX-ARHGAP) fusion gene affects GC. First, short hairpin RNA (shRNA) against BMX-ARHGAP or BMX-ARHGAP were introduced to treat SGC-7901 cells with the highest BMX-ARHGAP among the five GC cell lines (SGC-7901, MKN-45, NCI-N87, SNU-5, and AGS). Next, cell vitality, drug resistance, migration, and invasion of SGC-7901 cells, activities of Rho and JAK/STAT axis, as well as EMT and lymph node metastasis (LNM) were evaluated. The survival rate of the mice was then determined through the transfection of the specific pathogen-free NOD-SCID mice with treated SGC-7901 cells. The results showed that BMX-ARHGAP expression was associated with the infiltration degree of GC tumor and poor prognosis for patients with GC. BMX-ARHGAP silencing was found to play an inhibitory role in the Rho and JAK/STAT axis to reduce cell vitality, drug resistance, migration and invasion, reverse EMT process, as well as inhibit LNM. BMX-ARHGAP overexpression was observed to have induced effects on GC cells as opposed to those inhibited by BMX-ARHGAP silencing. The survival rate of mice was increased after transfection with silenced BMX-ARHGAP. These findings provided evidence that the suppression of BMX-ARHGAP resulted in the inhibition of RhoA to restraint the development of GC cells by blocking the JAK/STAT axis. 

Retracted: Yes

PubPeer comments:
  ,
Mechanochemical Synthesis of Poly(phenylene vinylenes)
Authors: Timothy M Swager
Jens B Ravnsb√¶k
Journal: ACS Macro Letters (2014)
Discipline: CHEMISTRY
Keywords: solid-state polymerization; poly(phenylene vinylenes); ball-milling; rapid process; molecular number average weights
Affiliations: Department of Chemistry, Massachusetts Institute of Technology, Massachusetts Avenue 77, Cambridge, Massachusetts 02139, United States

Abstract:  We report a simple, rapid, and solvent-free methodology for solid-state polymerizations yielding poly(phenylene vinylenes) (PPVs) promoted by ball-milling. This solid-state Gilch polymerization method produces PPVs in as little as five minutes of milling. Detailed investigations of the parameter space governing the solid-state polymerization, i.e., milling time, base strength, solid-state dilution, milling frequency, and size of milling balls, revealed that polymerization by ball-milling is a rapid process achieving molecular number average weights of up to 40 kDa in up to 70% yield. To explore the scope, a solid-state polymerization via the dithiocarbamate precursor route is explored. 

Retracted: No

PubPeer comments:
 Figure 2b appears to have a differential splice. Could the authors please post the uncropped original scans? *** Inverse, contrast enhanced  *** Original  ,
Biogenic amine production by the wine Lactobacillus brevis IOEB 9809 in systems that partially mimic the gastrointestinal tract stress
Authors: Andrea Romano
Pasquale Russo
Patrick Lucas
Pilar Fern√°ndez de Palencia
Giuseppe Spano
Mar√≠a Fern√°ndez
Paloma L√≥pez
Journal: BMC Microbiology (2012)
Discipline: MICROBIOLOGY
Keywords: fermented foods; biogenic amines; Lactobacillus brevis; tyramine; putrescine
Affiliations: Department of Molecular Microbiology and Infection Biology, Centro de Investigaciones Biol√≥gicas, C.S.I.C., Ramiro de Maeztu 9, Madrid 28040, Spain.

Abstract:  Background: Ingestion of fermented foods containing high levels of biogenic amines (BA) can be deleterious to human health. Less obvious is the threat posed by BA producing organisms contained within the food which, in principle, could form BA after ingestion even if the food product itself does not initially contain high BA levels. In this work we have investigated the production of tyramine and putrescine by Lactobacillus brevis IOEB 9809, of wine origin, under simulated gastrointestinal tract (GIT) conditions. Results: An in vitro model that simulates the normal physiological conditions in the human digestive tract, as well as Caco-2 epithelial human cell lines, was used to challenge L. brevis IOEB 9809, which produced both tyramine and putrescine under all conditions tested. In the presence of BA precursors and under mild gastric stress, a correlation between enhancement of bacterial survival and a synchronous transcriptional activation of the tyramine and putrescine biosynthetic pathways was detected. High levels of both BA were observed after exposure of the bacterium to Caco-2 cells. Conclusions: L. brevis IOEB 9809 can produce tyramine and putrescine under simulated human digestive tract conditions. The results indicate that BA production may be a mechanism that increases bacterial survival under gastric stress. 

Retracted: No

PubPeer comments:
  ,
Upregulation of CCT-3 Induces Breast Cancer Cell Proliferation Through miR-223 Competition and Wnt/Œ≤-Catenin Signaling Pathway Activation
Authors: Hongbo Qu
Huaying Dong
Mingli Han
Fang Zhu
Xiongqiang Hu
Journal: Frontiers in Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: CCT-3; Wnt/Œ≤-catenin; breast cancer; ceRNA; miR-223.
Affiliations: Department of Breast and Thyroid Surgery, The First People's Hospital of Chenzhou, Chenzhou, China., Department of Breast Health Center, The First People's Hospital of Chenzhou (South Hospital), Chenzhou, China., Department of General Surgery, Hainan General Hospital, Hainan Medical University, Haikou, China., Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Abstract:  The clinical significance and the function of chaperonin-containing TCP1 complex 3 (CCT-3) in breast cancer remain unknown. In this study, we found that CCT-3 was markedly overexpressed in breast cancer tissues. Statistical analysis revealed a significant correlation of CCT-3 expression with advanced breast cancer clinical stage and poorer survival. Ablation of CCT-3 knocked down the proliferation and the tumorigenicity of breast cancer cells in vitro and in vivo. CCT-3 may regulate breast cancer cell proliferation through a ceRNA network between miR-223 and Œ≤-catenin, thus affecting Wnt/Œ≤-catenin signaling pathway activation. We also validated that CCT-3 and Œ≤-catenin are novel direct targets of tumor suppressor miR-223. Our results suggest that both mRNA and the protein levels of CCT-3 are potential diagnosis biomarkers and therapeutic targets for breast cancer. 

Retracted: No

PubPeer comments:
 Fig 2A.  Ectopic miR-101-3p expression significantly inhibited the invasion of ACC cells, whereas miR-101-3p silencing (anti-miR-101-3p) enhanced the invasion of ACC cells . Fig 5D.  MiR-101-3p represses ACC cell proliferation and invasion by directly targeting Pim-1. ...D. Representative photographs of invaded cells .  ,
DcR3 induces proliferation, migration, invasion, and EMT in gastric cancer cells via the PI3K/AKT/GSK-3&beta;/&beta;-catenin signaling pathway
Authors: Dali An
Hua Ge
Shulin Ren
Chaosen Yue
Zhixia Li
Chaojie Liang
Jixiang Wu
Journal: OncoTargets and Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: DcR3; epithelial-mesenchymal transition; gastric cancer; metastasis.
Affiliations: Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, .

Abstract:  Background: Decoy receptor 3 (DcR3) has been reported to be overexpressed in a wide variety of malignancies and is correlated with tumorigenesis and progression. In gastric cancer (GC), DcR3 overexpression is associated with lymph node and distant metastasis, as well as poor prognosis. However, the functional role of DcR3 expression in GC remains elusive. Purpose: The aim of this study is to elucidate the direct role of DcR3 in regulating GC progression and metastasis and identify the potential mechanism. Methods: DcR3 expression was stably knocked down in HGC27 and MKN28 cells by transfecting the cells with DcR3 shRNA using lentiviral vector system. After the knockdown of DcR3 was confirmed, cell proliferation, colony formation, cell cycle distribution, apoptosis, cell invasion and migration were assessed in vitro. In addition, Western blot analysis was performed to evaluate the expression of downstream mediators of DcR3. Comparisons between multiple groups were performed using one-way analysis of variance (ANOVA) or unpaired Student's t-test. Differences were considered significant at P&lt;0.05. Results: Our findings demonstrate that DcR3 induces proliferation, migration, invasion, and promotes epithelial-mesenchymal transition (EMT) of GC cells. In addition, DcR3 increases the expression levels of several components of the PI3K/AKT/GSK-3Œ≤/Œ≤-catenin signaling pathway, such as p-AKT, GSK-3Œ≤, p-GSK-3Œ≤ and Œ≤-catenin. Additionally, DcR3 also enhances the expression of N-cadherin and Vimentin and decreases the expression of E-cadherin. Conclusion: In summary, the findings of this study indicate that during GC progression, DcR3 plays a key role in cell proliferation and invasion via the PI3K/AKT/GSK-3Œ≤/Œ≤-catenin signaling pathway. Thus, targeting DcR3 might be a potential therapeutic approach for the treatment of GC. 

Retracted: No

PubPeer comments:
 Figure 3D has an image in which features appear to be repeated (some after rotation). ***  ,
Dosage-dependent functions of fatty acid desaturase Ole1p in growth and morphogenesis of Candida albicans
Authors: Juliane Albert
Tulika Prasad
Shankarling Krishnamurthy
Joachim F Ernst
Rajendra Prasad
Arm√™l Plaine
Journal: Microbiology (2004)
Discipline: MICROBIOLOGY
Keywords: Candida albicans; virulence attributes; hyphal development; chlamydospore development; Ole1 fatty acid desaturase
Affiliations: Institut f√ºr Mikrobiologie, Heinrich-Heine-Universit√§t, 40225 D√ºsseldorf, Germany., Jawaharlal Nehru University, New Delhi 110067, India.

Abstract:  Conditions in the infected human host trigger virulence attributes of the fungal pathogen Candida albicans. Specific inducers and elevated temperatures lead to hyphal development or regulate chlamydospore development. To explore if these processes are affected by membrane lipids, an investigation of the functions of the Ole1 fatty acid desaturase (stearoyl-CoA desaturase) in C. albicans, which synthesizes oleic acid, was undertaken. A conditional strain expressing OLE1 from the regulatable MET3 promoter was unable to grow in repressing conditions, indicating that OLE1 is an essential gene. In contrast, a mutant lacking both alleles of OLE2, encoding a Ole1p homologue, was viable and had no apparent phenotypes. Partial repression of MET3p-OLE1 slightly lowered oleic acid levels and decreased membrane fluidity; these conditions permitted growth in the yeast form, but prevented hyphal development in aerobic conditions and blocked the formation of chlamydospores. In contrast, in hypoxic conditions, which trigger an alternative morphogenetic pathway, hyphal morphogenesis was unaffected. Because aerobic morphogenetic signalling and oleic acid biosynthesis require oxygen, it is proposed that oleic acid may function as a sensor activating specific morphogenetic pathways in normoxic conditions. 

Retracted: No

PubPeer comments:
 In this article Y Yazdanpanah did not declare any competing interests However he has some  , 
 In this article Yazdanpanah did not declare any competing interests. However he has some.  , 
 Eric: Could you elaborate please? Journal policy: https: www.elsevier.com journals anaesthesia-critical-care-and-pain-medicine 2352-5568 guide-for-authors ***  ,
Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity
Authors: Wenjun Song
Patrick Poquiz
Mahmoud A Pouladi
Robert Schwarzenbacher
Mark Ellisman
Jonathan Tjong
Eva Klinglmayr
Michael R Hayden
Isabelle Rouiller
Guy Perkins
Geraldine Liot
Blaise Bossy
Ella Bossy-Wetzel
Jin Chen
Yue Zhou
Alejandra Petrilli
Eliezer Masliah
Journal: Nature Medicine (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Huntington's disease; neurodegenerative disorder; polyglutamine expansion; huntingtin; mitochondrial dysfunction
Affiliations: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.

Abstract:  Huntington's disease is an inherited and incurable neurodegenerative disorder caused by an abnormal polyglutamine (polyQ) expansion in huntingtin (encoded by HTT). PolyQ length determines disease onset and severity, with a longer expansion causing earlier onset. The mechanisms of mutant huntingtin-mediated neurotoxicity remain unclear; however, mitochondrial dysfunction is a key event in Huntington's disease pathogenesis. Here we tested whether mutant huntingtin impairs the mitochondrial fission-fusion balance and thereby causes neuronal injury. We show that mutant huntingtin triggers mitochondrial fragmentation in rat neurons and fibroblasts of individuals with Huntington's disease in vitro and in a mouse model of Huntington's disease in vivo before the presence of neurological deficits and huntingtin aggregates. Mutant huntingtin abnormally interacts with the mitochondrial fission GTPase dynamin-related protein-1 (DRP1) in mice and humans with Huntington's disease, which, in turn, stimulates its enzymatic activity. Mutant huntingtin-mediated mitochondrial fragmentation, defects in anterograde and retrograde mitochondrial transport and neuronal cell death are all rescued by reducing DRP1 GTPase activity with the dominant-negative DRP1 K38A mutant. Thus, DRP1 might represent a new therapeutic target to combat neurodegeneration in Huntington's disease. 

Retracted: No

PubPeer comments:
null, 
 The information needed to draw the conclusion given in the title of the paper is absent from the paper. DRP-1 was only tested at a single molar ratio (0.5 u03bcM DRP-1: 0.4 u03bcM of GST-HTT). The claim made in the title of the paper is ***necessarily*** an assertion that the activity of a given concentration of DRP-1 will increase as the molar ratio of HTT (or mutant HTT) is increased. Yet, No such data is given! , 
 [](http: )https: www.ncbi.nlm.nih.gov pmc articles PMC3051025 bin NIHMS265991-supplement-1.pdf  ,
Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes
Authors: Hiroko Miyahara
Akimasa Hatanaka
Zhi-Hong Yang
Journal: Lipids in Health and Disease (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Palmitoleic acid; diabetes; insulin resistance; beta-cell apoptosis; KK-Ay mice
Affiliations: Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo 192-0991, Japan. 

Abstract:  Background: Studies have demonstrated the beneficial effect of palmitoleic acid (C16:1 n-7) on reducing muscle insulin resistance and preventing beta-cell apoptosis. However, the effect of palmitoleic acid on diabetes remains to be elucidated. The aim of this study was to examine the antidiabetic effect of palmitoleic acid in KK-Ay mice, a spontaneous model for studies of obese type 2 diabetes with low insulin sensitivity. Methods: KK-Ay mice were orally administered vehicle, 300 mg/kg of palmitoleic acid, or 300 mg/kg of palmitic acid (C16:0) on a daily basis for 4 weeks. Results: Palmitoleic acid reduced body weight increase, ameliorated the development of hyperglycemia and hypertriglyceridemia, and improved insulin sensitivity. In addition, hepatic characteristics were significantly affected, as weight of the liver and hepatic triglyceride levels were lower in the palmitoleic acid group when compared to the control (vehicle and palmitic acid groups). Oil red O staining clearly indicated reduced hepatic lipid accumulation in response to palmitoleic acid. Furthermore, palmitoleic acid down-regulated mRNA expressions of proinflammatory adipocytokine genes (TNFŒ± and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver. Conclusions: These results suggest that palmitoleic acid improves hyperglycemia and hypertriglyceridemia by increasing insulin sensitivity, in part owing to suppressing proinflammatory gene expressions and improving hepatic lipid metabolism in diabetic mice. 

Retracted: No

PubPeer comments:
 2020 retraction. https: nanoscalereslett.springeropen.com articles 10.1186 s11671-019-3234-1 The Editors-in-Chief have retracted this article [1] because it significantly overlaps with a previously published article by the same authors [2]. The authors agree with this retraction. References 1. Sun B, Wang Y, Ding G (2016) Flexible Field Emitter for X-ray Generation by Implanting CNTs into Nickel Foil. Nanoscale Res Lett 11:326 https: doi.org 10.1186 s11671-016-1523-5 2. Sun B, Wang Y, Ding G (2016) Fabrication of a Ni-matrix CNT flexible field emission electron source for X-ray generation by micromachining. Opt Mater Express 6:2304u20132312 https: doi.org 10.1364 OME.6.002304 ,
MicroRNA‚Ä?36 directly targets Sox‚Ä? in osteosarcoma to inhibit tumorigenesis
Authors: Tianding Wu
Hongbin Lu
Dongzhe Li
Jianzhong Hu
Yong Cao
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: microRNAs; miR‚Ä?36; osteosarcoma; tumorigenesis; gene expression
Affiliations: Department of Spine Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  Previous evidence has suggested that microRNAs (miRNAs or miRs), which belong to a class of non‚Äëcoding RNAs, shape cellular processes by regulating gene expression. Abnormal expression of miRNAs has been associated with tumorigenesis in multiple cancers. However, the function of miR‚Ä?36 in osteosarcoma (OS) remains unknown. The experimental procedures used in the present study included flow cytometry, reverse transcription‚Äëquantitative polymerase chain reaction, luciferase reporter assay, invasion assay, western blot analysis and in vivo implantation. The results of the present study demonstrated that miR‚Ä?36 may serve as a tumor suppressor in OS. Downregulation of miR‚Ä?36 was observed in human OS specimens as well as OS cell lines. In addition, a significant negative correlation between sex determining region Y‚Äëbox 2 (Sox‚Ä?) expression and miR‚Ä?36 was demonstrated. miR‚Ä?36 was confirmed to target the 3'‚Äëuntranslated region of Sox‚Ä? to inhibit proliferation, migration and invasion of OS cells. Consistently, restoration of Sox‚Ä? expression counteracted the effect of miR‚Ä?36, and recovered the tumorigenic potential of OS cells. The present study established a novel association between miR‚Ä?36 and Sox‚Ä? in OS. This relationship between miR‚Ä?36 and Sox‚Ä? may lead to improved knowledge concerning OS progression and sheds light on potential novel therapeutic interventions for OS treatment. 

Retracted: No

PubPeer comments:
 Expression of deepest concern: Figure 1C: H1299: Microscopy data has been duplicated and presented as something else. Figure 1C: U2-OS: Two cases where microscopy data has been duplicated and presented as something else in Figure 3E. Figure 3E: H1299: two cases where microscopy data has been duplicated and presented as something else. Figure 7G: two cases where microscopy data has been duplicated and presented as something else.  , 
 #1 Thank you. We are checking the original data and will contact the journal. , 
 Additional issue with 7G. ***  ,
Retracted Article: Exosome-derived PTENP1 suppresses cisplatin resistance of bladder cancer (BC) by suppressing cell proliferation, migration and inducing apoptosis via the miR-103a/PDCD4 axis
Authors: Diao Yuan
Yunju Zi
Xiaowen Liu
Yu Lu
Fengyu Chen
Xiang He
Xingre Lu
Journal: RSC Advances (2019)
Discipline: CHEMISTRY
Keywords: Bladder cancer; Chemotherapy drug resistance; PTEN pseudogene-1; PTENP1; Serum exosomes
Affiliations: Department of Clinical Laboratory, The People's Hospital of Wenshan Prefecture in Yunnan Province, Wenshan, China

Abstract:  Bladder cancer (BC) is a lethal cancer that threatens the health of millions of people. Chemotherapy drug resistance, for example, cisplatin (DDP) resistance, is a huge limitation for BC therapy. PTEN pseudogene-1 (PTENP1) has been identified as a significant biomarker of multiple cancers. Therefore, it is essential to illuminate the molecular mechanism of PTENP1 in BC cell DDP resistance and progression. Serum exosomes were isolated using an ExoQuick precipitation kit. Serum exosomes were round-shaped vesicles of 100 ¬± 60 nm in size. The expression of PTENP1 was down-regulated in serum exosomes isolated from cisplatin non-responsive patients compared with responsive patients. ROC curves certified the diagnostic value of PTENP1. Apparently, PTENP1 transfection inhibited DDP-resistant BC cell proliferation, migration, cisplatin resistance and facilitated apoptosis. Next, we discovered that PTENP1 was a sponge of miR-103a, while PDCD4 was a target of miR-103a. More importantly, PTENP1 regulated DDP-resistant cell viability, migration, apoptosis and cisplatin resistance by interacting with the miR-103a/PDCD4 axis. In addition, PTENP1 hindered tumor growth of cisplatin-resistant mice. Exosome-derived PTENP1 suppressed the DDP resistance of BC by inhibiting cell proliferation, migration and promoting apoptosis through regulating the miR-103a/PDCD4 axis, representing a targeted therapy for DDP-resistant BC patients. 

Retracted: Yes

PubPeer comments:
 This article has been retracted: https: pubs.rsc.org en content articlelanding 2021 ra d1ra90073k#!divAbstract , 
 This article should never have been considered in a serious journal. A quick look at the affiliations and first figure should be enough: Gibberish email address Nonsense EM micrographs of  exosomes A CD63 immunoblot that cannot be real (CD63 should be smeared). , 
 A study like this one that uses only polymer precipitation as an isolation method is not about exosomes at all. Exosomes are extracellular vesicles (EVs) from the endosomal system, and they have similar size and other characteristics as EVs from the cell s plasma membrane. Polymer precipitation concentrates particulate matter. If used with serum, almost all of the precipitated material will be non-EV particles like lipoproteins. There will be a few EVs, and you can certainly get a signal for tetraspanins, but that doesn t say anything about purity. Characterization methods like NTA are general particle tracking methods and are not specific to exosomes or other EVs. See also https: www.tandfonline.com doi full 10.1080 20013078.2018.1535750 ,
Nox2 dependent redox-regulation of microglial response to amyloid-Œ≤ stimulation and microgliosis in aging
Authors: Fangfei Liu
Jian -Mei Li
Colin Smith
Lampson M Fan
Li Geng
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Microglia; Nox2 enzyme; neuroinflammation; reactive oxygen species; ROS
Affiliations: School of Biological Sciences, University of Reading, Reading, UK., Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK., Faculty of Cardiovascular Medicine, University of Oxford, Oxford, UK., Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK., School of Biological Sciences, University of Reading, Reading, UK. ., Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK. .

Abstract:  Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen species (ROS). Amyloid Œ≤ (AŒ≤) plays a crucial role in Alzheimer's disease. However, the mechanism of AŒ≤-induced microglial dysfunction and redox-regulation of microgliosis in aging remains unclear. In this study, we examined Nox2-derived ROS in mediating microglial response to AŒ≤ peptide 1-42 (AŒ≤42) stimulation in vitro, in aging-associated microgliosis in vivo and in post-mortem human samples. Compared to controls, AŒ≤42 markedly induced BV2 cell ROS production, Nox2 expression, p47phox and ERK1/2 phosphorylation, cell proliferation and IL-1Œ≤ secretion. All these changes could be inhibited to the control levels in the presence of Nox2 inhibitor or superoxide scavenger. Compared to young (3-4 months) controls, midbrain tissues from wild-type aging mice (20-22 months) had significantly higher levels of Nox2-derived ROS production, AŒ≤ deposition, microgliosis and IL-1Œ≤ production. However, these aging-related changes were reduced or absent in Nox2 knockout aging mice. Clinical significance of aging-associated Nox2 activation, microgliosis and IL-1Œ≤ production was investigated using post-mortem midbrain tissues of humans at young (25-38 years) and old age (61-85 years). In conclusion, Nox2-dependent redox-signalling is crucial in microglial response to AŒ≤42 stimulation and in aging-associated microgliosis and brain inflammation. 

Retracted: No

PubPeer comments:
 Figure 3A. * Red boxes: The Iba-1 (20 kDa) and P-p47phox (50 kDa) panels look more similar than expected.  The Supplemental materials provide for the uncropped blots, and there the similarities are even more clear. Of concern, the two blots are cropped differently, to enhance the supposedly different sizes of the marked protein bands.  ,
Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactions
Authors: Chang-Fu Peng
Peiyee Lee
Stanley J Korsmeyer
Young-Jae Nam
Yukihiro Hayakawa
Kartik Mani
Anthony W Ashton
Barath Krishnamurthy
Richard N Kitsis
Journal: Molecular Cell (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Death-fold domains; apoptosis; CARD; DD; DED
Affiliations: Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.

Abstract:  Death-fold domains constitute an evolutionarily conserved superfamily that mediates apoptotic signaling. These motifs, including CARD (caspase recruitment domain), DD (death domain), and DED (death effector domain), are believed to exert their effects solely through homotypic interactions. Herein we demonstrate that the CARD-containing protein ARC engages in nontraditional death-fold interactions to suppress both extrinsic and intrinsic death pathways. The extrinsic pathway is disrupted by heterotypic interactions between ARC's CARD and the DDs of Fas and FADD, which inhibit Fas-FADD binding and assembly of the death-inducing signaling complex (DISC). The intrinsic pathway is antagonized by ARC-Bax binding, involving ARC's CARD and the Bax C terminus. This inhibits Bax activation and translocation to the mitochondria. Knockdown of endogenous ARC facilitates DISC assembly and triggers spontaneous Bax activation and apoptosis. Conversely, physiological levels of ARC suppress these events. These studies establish a critical role for nonhomotypic death-fold interactions in the regulation of apoptosis. 

Retracted: No

PubPeer comments:
  , 
 ERRATUM| AUGUST 27, 2020 In Figure 6E on page 2040, the wrong image is shown for spectratype IV. The corrected Figure 6E is shown below. The error does not change the interpretation of the findings of the study.  ,