PReD-Bench/PRed-Bench huggingface dataset:
Visualization of T Cell Migration in the Spleen Reveals a Network of Perivascular Pathways that Guide Entry into T Zones
Authors: Sarah Wideman
Jens Rittscher
Tal I Arnon
Anne Chauveau
Hung-Wei Cheng
Felix Y Zhou
Burkhard Ludewig
Angelina De Martin
Gabriela Pirgova
Journal: Immunity (2020)
Discipline: IMMUNOLOGY
Keywords: GPCRs; T cells; bridging channels; intravital imaging; lymphocyte trafficking
Affiliations: University of Oxford, Kennedy Institute of Rheumatology, OX3 7FY Oxford, UK., Institute of Immunobiology, Kantonsspital St. Gallen, 9007 St. Gallen, Switzerland., University of Oxford, Ludwig Institute for Cancer Research, OX3 7DQ Oxford, UK., University of Oxford, Ludwig Institute for Cancer Research, OX3 7DQ Oxford, UK; University of Oxford, Institute of Biomedical Engineering, OX3 7DQ Oxford, UK; University of Oxford, Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, OX3 7XP Oxford, UK., University of Oxford, Kennedy Institute of Rheumatology, OX3 7FY Oxford, UK. Electronic address: .

Abstract:  Lymphocyte homeostasis and immune surveillance require that T and B cells continuously recirculate between secondary lymphoid organs. Here, we used intravital microscopy to define lymphocyte trafficking routes within the spleen, an environment of open blood circulation and shear forces unlike other lymphoid organs. Upon release from arterioles into the red pulp sinuses, T cells latched onto perivascular stromal cells in a manner that was independent of the chemokine receptor CCR7 but sensitive to Gi protein-coupled receptor inhibitors. This latching sheltered T cells from blood flow and enabled unidirectional migration to the bridging channels and then to T zones, entry into which required CCR7. Inflammatory responses modified the chemotactic cues along the perivascular homing paths, leading to rapid block of entry. Our findings reveal a role for vascular structures in lymphocyte recirculation through the spleen, indicating the existence of separate entry and exit routes and that of a checkpoint located at the gate to the T zone. 

Retracted: No

PubPeer comments:
 In Figure 5H the mean and error bars do not seem to overlap with the datapoints at all. Probably an honest mistake because the effect seems even stronger when the error bars would be at the correct place, however I think it should be corrected. , 
 #1 Thanks for this note. Yes, this was an editing mistake we accidentally introduced in the last version we uploaded. We have contacted the journal about this a few months back, so hopefully we can fix it. ,
Luminal iron levels govern intestinal tumorigenesis after Apc loss in vivo
Authors: Sorina Radulescu
Rachel A Ridgway
Chris Tselepis
Pedro Salgueiro
Owen J Sansom
Daniel H Stones
Ewan McGhee
Samuel J Ford
Tariq H Iqbal
Matthew J Brookes
Kurt Anderson
Journal: Cell Reports (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: iron; colorectal cancer; mechanism; cellular iron acquisition proteins; TfR1
Affiliations: Beatson Institute of Cancer Research, Glasgow, UK.

Abstract:  It is clear from epidemiological studies that excess iron is associated with increased risk of colorectal cancer; however, questions regarding the mechanism of how iron increases cancer risk, the source of the excess iron (circulating or luminal), and whether iron reduction represents a potential therapeutic option remain unanswered. In this study, we show that after Apc deletion, the cellular iron acquisition proteins TfR1 and DMT1 are rapidly induced. Conversely, restoration of APC reduces cellular iron due to repression of these proteins. To test the functional importance of these findings, we performed in vivo investigations of the impact of iron levels on intestinal tumorigenesis. Strikingly, depletion of luminal (but not systemic) iron strongly suppressed murine intestinal tumorigenesis, whereas increased luminal iron strongly promoted tumorigenesis. Taken together, our data definitively delineate iron as a potent modifier of intestinal tumorigenesis and have important implications for dietary iron supplementation in patients at high risk of colorectal cancer. 

Retracted: No

PubPeer comments:
 Several people tagged me about the following on Twitter. I will admit that I do not understand enough about the methods applicable to this table to know if this is an expected measurement. In Table 3, two columns show the exact same numbers and percentages. Is this expected? The text says  confirming that the propensity matched groups have identical underlying patient characteristics. so it sounds like this is expected, but it is very rare to see tables with different patient groups with the same exact percentages. ![file] , 
 #1 More problematic the fact that 77.1% of the patients who received HCQ also received steroids while only 36.5% of the patients not receiving HCQ, received steroids. Given the positive effect of steroids on Covid patients, this single fact makes this study highly poorly designed. ,
A novel mechanism of plasminogen activation in epithelial and mesenchymal cells
Authors: Andra Sterea
David M Waisman
Moamen Bydoun
Ian C G Weaver
Alamelu G Bharadwaj
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Cancer dissemination; EMT; proteases; plasmin; matrix remodeling
Affiliations: Department of Pathology, Halifax, Nova Scotia, Canada., Department of Physiology and Biophysics, Halifax, Nova Scotia, Canada., Department of Psychology and Neuroscience, Halifax, Nova Scotia, Canada., Department of Psychiatry, Halifax, Nova Scotia, Canada., Brain Repair Centre, Dalhousie University, Halifax, Nova Scotia, Canada., Department of Biochemistry and Molecular Biology, Halifax, Nova Scotia, Canada., Department of Pathology, Halifax, Nova Scotia, Canada. ., Department of Biochemistry and Molecular Biology, Halifax, Nova Scotia, Canada. .

Abstract:  Cancer dissemination is initiated by the movement of cells into the vasculature which has been reported to be triggered by EMT (epithelial to mesenchymal transition). Cellular dissemination also requires proteases that remodel the extracellular matrix. The protease, plasmin is a prominent player in matrix remodeling and invasion. Despite the contribution of both EMT and the plasminogen activation (PA) system to cell dissemination, these processes have never been functionally linked. We reveal that canonical Smad-dependent TGFβ1 signaling and FOXC2-mediated PI3K signaling in cells undergoing EMT reciprocally modulate plasminogen activation partly by regulating the plasminogen receptor, S100A10 and the plasminogen activation inhibitor, PAI-1. Plasminogen activation and plasminogen-dependent invasion were more prominent in epithelial-like cells and were partly dictated by the expression of S100A10 and PAI-1. 

Retracted: No

PubPeer comments:
 I have noticed some potential issues with some of the blot figures. ![file] Some of the bands appear to be duplicated. The bands for B-actin and GAPDH are the same (Fig 3a and Fig 3f) ![file] Likewise, a band for B-actin in two experiments figures (Figure 1b and Figure 4e) ,
Role of fibroblast growth factor 21 (FGF21) in undernutrition-related attenuation of growth in mice
Authors: Rita Ann Kubicky
Shufang Wu
Alexei Kharitonenkov
Francesco De Luca
Journal: Endocrinology (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Caloric intake; Skeletal growth; GH insensitivity; Fibroblast growth factor 21 (FGF21); Mice
Affiliations: Section of Endocrinology and Diabetes, St. Christopher's Hospital for Children, Drexel University College of Medicine, Philadelphia, Pennsylvania 19134, USA., Section of Endocrinology and Diabetes (R.A.K., S.W., F.D.L.), St. Christopher's Hospital for Children, Drexel University College of Medicine, Philadelphia, Pennsylvania 19134, Lilly Research Laboratories (A.K.), Indianapolis, Indiana 46285

Abstract:  Reduced caloric intake in mammals causes reduced skeletal growth and GH insensitivity. However, the underlying molecular mechanisms are not fully elucidated. The aim of this study was to determine whether the increased activity of fibroblast growth factor 21 (FGF21) during chronic undernutrition in mice causes GH insensitivity and growth failure. After 4 wk of food restriction, fgf21 knockout (KO) mice exhibited greater body and tibial growth than their wild-type (WT) littermates. Daily injections of recombinant human FGF21 in a subgroup of food-restricted fgf21 KO mice prevented these differences in body and tibial growth. At the end of the 4-wk food restriction, GH binding and GH receptor expression were reduced in the liver and in the growth plate of food-restricted WT mice (compared to WT mice fed ad libitum), whereas they were similar between food-restricted and ad libitum KO mice. In addition, a single injection of GH induced greater liver signal transducer and activator of transcription 5 phosphorylation and IGF-I mRNA in food-restricted KO mice than in WT mice. Lastly, in the tibial growth plate of food-restricted WT mice, FGF21 mRNA and protein expression was greater than that of WT mice fed ad libitum. In contrast, the IGF-I mRNA and protein expression was smaller. Our findings support a causative role for FGF21 in the inhibition of skeletal growth during prolonged undernutrition. Such role may be mediated by the antagonistic effect of FGF21 on GH action in the liver and, possibly, in the growth plate. 

Retracted: No

PubPeer comments:
 Figure 4A. much more similar than you would expect. https: imgur.com cjDwCFh , 
 #1 I agree with the original poster and also believe there may be an unexpectedly similar portion of the bands displayed in the upper right panel of Figure 4A. Shown below with original and false color. Some of these authors withdrew another paper due to similar issues, discussed here: https: pubpeer.com publications 70278FC3FE87F93815BA3DF7D59B51#2. *** ![file] ,
Zinc finger protein ZBTB20 expression is increased in hepatocellular carcinoma and associated with poor prognosis
Authors: Wei-ping Zhang
Hong-yang Wang
Li-wei Dong
Qing Wang
Liang Tang
Ye-xiong Tan
Zhi-fang Xie
He-ping Hu
Yi-bin Ren
Dan Cao
Journal: BMC Cancer (2011)
Discipline: CLINICAL MEDICINE
Keywords: ZBTB20; hepatocellular carcinoma; prognosis; expression levels; liver-specific genes
Affiliations: International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, the Second Military Medical University, 225 Changhai Road, Shanghai, 200433, PR China.

Abstract:  Background: Our previous studies showed that ZBTB20, a new BTB/POZ-domain gene, could negatively regulate α feto-protein and other liver-specific genes, concerning such as bio-transformation, glucose metabolism and the regulation of the somatotropic hormonal axis. The aim of this study is to determine the potential clinical implications of ZBTB20 in hepatocellular carcinoma (HCC). Methods: Quantitative real-time RT-PCR and Western blot analyses were used to detect expression levels of ZBTB20 in 50 paired HCC tumorous and nontumorous tissues and in 20 normal liver tissues. Moreover, expression of ZBTB20 was assessed by immunohistochemistry of paired tumor and peritumoral liver tissue from 102 patients who had undergone hepatectomy for histologically proven HCC. And its relationship with clinicopathological parameters and prognosis was investigated. Results: Both messenger RNA and protein expression levels of ZBTB20 were elevated significantly in HCC tissues compared with the paired non-tumor tissues and normal liver tissues. Overexpressed ZBTB20 protein in HCC was significantly associated with vein invasion (P=0.016). Importantly, the recurrence or metastasis rates of HCCs with higher ZBTB20 expression were markedly greater than those of HCCs with lower expression (P=0.003, P=0.00015, respectively). Univariate and multivariate analyses revealed that ZBTB20 overexpression was an independent prognostic factor for HCC. The disease-free survival period and over-all survival period in patients with overexpressed ZBTB20 in HCC was significantly reduced. Conclusions: The expression of ZBTB20 is increased in HCC and associated with poor prognosis in patients with HCC, implicating ZBTB20 as a candidate prognostic marker in HCC. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Macrophagic myofasciitis: characterization and pathophysiology
Authors: F J Authier
R K Gherardi
Journal: Lupus (2012)
Discipline: CLINICAL MEDICINE
Keywords: Aluminium oxyhydroxide; vaccines; adjuvant effect; immune responses; health problems
Affiliations: AP-HP, Hôpital H. Mondor, France.

Abstract:  Aluminium oxyhydroxide (alum), a nanocrystalline compound forming agglomerates, has been used in vaccines for its immunological adjuvant effect since 1927. Alum is the most commonly used adjuvant in human and veterinary vaccines, but the mechanisms by which it stimulates immune responses remain incompletely understood. Although generally well tolerated, alum may occasionally cause disabling health problems in presumably susceptible individuals. A small proportion of vaccinated people present with delayed onset of diffuse myalgia, chronic fatigue and cognitive dysfunction, and exhibit very long-term persistence of alum-loaded macrophages at the site of previous intramuscular (i.m.) immunization, forming a granulomatous lesion called macrophagic myofasciitis (MMF). Clinical symptoms associated with MMF are paradigmatic of the recently delineated 'autoimmune/inflammatory syndrome induced by adjuvants' (ASIA). The stereotyped cognitive dysfunction is reminiscent of cognitive deficits described in foundry workers exposed to inhaled Al particles. Alum safety concerns will largely depend on whether the compound remains localized at the site of injection or diffuses and accumulates in distant organs. Animal experiments indicate that biopersistent nanomaterials taken up by monocyte-lineage cells in tissues, such as fluorescent alum surrogates, can first translocate to draining lymph nodes, and thereafter circulate in blood within phagocytes and reach the spleen, and, eventually, slowly accumulate in the brain. 

Retracted: No

PubPeer comments:
 In Figure 5a, the blood vessels are very different when comparing the different time points (0-21 d). This indicates that different animals have been analyzed and any comparison is invalid. ![file] , 
 Thanks a lot for the comment. We studied the hydrogel degradation behavior in vivo by subcutaneous injection of the hydrogels into different rats. The hydrogel status in different rats was observed at different time points. Therefore, the blood vessels were different at different time points. Even though the degradation of the hydrogels in different rats may be somewhat different due to the individual difference, we performed the hydrogel degradation experiment in three separate tests at each time point, which may indicate reasonably the degradation trend of the hydrogels in vivo. The representative images for the hydrogel status at different time points are shown in Figure 5a, and the average weights of the hydrogels at various time points are shown in Figure 5b. Thanks a lot. ,
Chromium Supplementation and the Effects on Metabolic Status in Women with Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial
Authors: Mehri Jamilian
Zatollah Asemi
Journal: Annals of Nutrition and Metabolism (2015)
Discipline: CLINICAL MEDICINE
Keywords: Chromium intake; insulin metabolism; lipid profiles; polycystic ovary syndrome; randomized trial

Abstract:  Background: The aim of the present study was to evaluate the beneficial effects of chromium intake on markers of insulin metabolism and lipid profiles in women with polycystic ovary syndrome (PCOS). Methods: In a prospective, randomized, double-blind, placebo-controlled trial, 64 women with PCOS were randomized to receive 200 µg chromium picolinate supplements (n = 32) or placebo (n = 32) for 8 weeks. Fasting blood samples were obtained at baseline and 8 weeks after the intervention to quantify markers of insulin metabolism and lipid concentrations. Results: Chromium supplementation in women with PCOS resulted in significant decreases in serum insulin levels (-3.6 ± 7.4 vs. +3.6 ± 6.2 µIU/ml, p &lt; 0.001), homeostasis model of assessment-insulin resistance (HOMA-IR; -0.8 ± 1.6 vs. +0.9 ± 1.5, p &lt; 0.001), homeostatic model assessment-beta cell function (HOMA-B; -15.5 ± 32.3 vs. +13.6 ± 23.1, p &lt; 0.001), and a significant increase in quantitative insulin sensitivity check index (QUICKI) score (+0.02 ± 0.03 vs. -0.008 ± 0.02, p = 0.001) compared with the placebo. In addition, a trend toward a significant effect of chromium supplementation on decreasing serum triglycerides (-12.4 ± 74.4 vs. +15.2 ± 32.4 mg/dl, p = 0.05), very low-density lipoprotein-cholesterol (-2.5 ± 14.9 vs. +3.0 ± 6.5 mg/dl, p = 0.05), and cholesterol concentrations (-8.6 ± 21.9 vs. +0.7 ± 22.4 mg/dl, p = 0.09) was seen. Conclusions: Eight weeks of chromium supplementation among PCOS women had favorable effects on markers of insulin metabolism. 

Retracted: No

PubPeer comments:
 Fig 3A shows anomalies that cannot be easily explained as gel artifacts. The alleged 8hr time point (STAT3 panel) has an additional band running across half lane that is not visible in any of the other panels. Also, there is a dot between lane 3 and 4 which is not visible in the other panels (dots between other lanes however run across panels. Also, there is a rather obvious splice line running through the middle of lane 3 in the Smad1 panel. Providing the original blots may clarify the situation. ![image] ,
MDM2-dependent downregulation of p21 and hnRNP K provides a switch between apoptosis and growth arrest induced by pharmacologically activated p53
Authors: Elisabeth Hedström
Wenjie Bao
Galina Selivanova
Abdeladim Moumen
Martin Enge
Stephen P Jackson
Journal: Cancer Cell (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p53; RITA; apoptosis; MDM2; p21
Affiliations: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden.

Abstract:  We have previously identified the p53-reactivating compound RITA in a cell-based screen. Here, using microarray analysis, we show that the global transcriptional response of tumor cells to RITA is p53 dependent. Pathway analysis revealed induction of the p53 apoptosis pathway, consistent with apoptosis being the major response to RITA in cancer cells. We uncovered that MDM2 released from p53 by RITA promotes degradation of p21 and the p53 cofactor hnRNP K, required for p21 transcription. Functional studies revealed MDM2-dependent inhibition of p21 as a key switch regulating cell fate decisions upon p53 reactivation. Our results emphasize the utility of targeting wild-type p53 protein itself as a promising approach for anticancer therapy. 

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 A120 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 ,
Synergistic and Superimposed Effect of Bone Marrow-Derived Mesenchymal Stem Cells Combined with Fasudil in Experimental Autoimmune Encephalomyelitis
Authors: Wan-Fang Yang
Jian-Chun Liu
Guo-Bin Song
Qing Wang
Cun-Gen Ma
Chun-Yun Liu
Jing-Wen Yu
Hai-Fei Zhang
Yan-Hua Li
Bao-Guo Xiao
Jie-Zhong Yu
Ya-Ping Yan
Journal: Journal of Molecular Neuroscience (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Experimental autoimmune encephalomyelitis; Fasudil; Mesenchymal stem cells; Rho kinase inhibitor.
Affiliations: Department of Neurology, Institute of Brain Science, Medical School, Shanxi Datong University, Datong, China., "2011" Collaborative Innovation Center/Research Center of Neurobiology, Shanxi University of Traditional Chinese Medicine, Taiyuan, China., Neurological Institute, Tianjin Medical University General Hospital of Tianjin Medical University, Tianjin, China., Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China. ., Department of Neurology, Institute of Brain Science, Medical School, Shanxi Datong University, Datong, China. ., "2011" Collaborative Innovation Center/Research Center of Neurobiology, Shanxi University of Traditional Chinese Medicine, Taiyuan, China. .

Abstract:  Bone marrow-derived mesenchymal stem cells (MSCs) are the ideal transplanted cells of cellular therapy for promoting neuroprotection and neurorestoration. However, the optimization of transplanted cells and the improvement of microenvironment around implanted cells are still two critical challenges for enhancing therapeutic effect. In the current study, we observed the therapeutic potential of MSCs combined with Fasudil in mouse model of experimental autoimmune encephalomyelitis (EAE) and explored possible mechanisms of action. The results clearly show that combined intervention of MSCs and Fasudil further reduced the severity of EAE compared with MSCs or Fasudil alone, indicating a synergistic and superimposed effect in treating EAE. The addition of Fasudil inhibited MSC-induced inflammatory signaling TLR-4/MyD88 and inflammatory molecule IFN-γ, IL-1β, and TNF-α but did not convert M1 microglia to M2 phenotype. The delivery of MSCs enhanced the expression of glial cell-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) compared with that of Fasudil. Importantly, combined intervention of MSCs and Fasudil further increased the expression of BDNF and GDNF compared with the delivery of MSCs alone, indicating that combined intervention of MSCs and Fasudil synergistically contributes to the expression of neurotrophic factors which should be related to the expression of increased galactocerebroside (GalC) compared with mice treated with Fasudil and MSCs alone. However, a lot of investigation is warranted to further elucidate the cross talk of MSCs and Fasudil in the therapeutic potential of EAE/multiple sclerosis. 

Retracted: No

PubPeer comments:
 Figure 4a, 6, and 7a use the same beta-Actin bands : ![file] ,
Tetrodotoxin attenuates isoproterenol-induced hypertrophy in H9c2 rat cardiac myocytes
Authors: Hui Li
Feng-Lan Li
Qing-Ting Bu
Er-Fu Chu
Mei-Na Sun
Shu-Chao Pang
Ming-Zi Chen
Journal: Molecular and Cellular Biochemistry (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cardiac hypertrophy; sympathetic drive; cardiomyocyte hypertrophy; sodium channel blocker; tetrodotoxin
Affiliations: Department of Biochemistry and Molecular Biology, Basic Medical Science College, Harbin Medical University, No. 194 Xue-fu Road, Nan-gang District, Harbin 150081, Heilongjiang, People's Republic of China.

Abstract:  Cardiac hypertrophy is often associated with an increased sympathetic drive, and both in vitro and in vivo studies have demonstrated the development of cardiomyocyte hypertrophy in response to either α- or β- adrenergic stimulation. The present study was carried out to determine whether the reversible sodium channel blocker tetrodotoxin (TTX) exerts a direct anti-hypertrophic effect on isoproterenol (ISO)-induced cell hypertrophy and find the underlying mechanism that regulate [Na(+)]( i ). The experiments were performed on cultured H9c2 cells exposed to ISO (10 μM) alone or combined with TTX (1 μM) for 48 h. Our results showed that ISO significantly increased cell surface area by 30 % and atrial natriuretic peptide gene expression by nearly twofold (p &lt; 0.05 for both). These effects were associated with a significant reduction in the gene expression of Na(+)/K(+)-ATPase isoforms α2 and α3, whereas the α1 isoform was unaffected. Conversely, ISO increased Na(+)-H(+) exchanger 1 (NHE-1) gene expression by approximately 40 % and significantly increased [Na(+)]( i ) level by 50 % (p &lt; 0.05 for both). ISO was also found to significantly increase aquaporin 4 gene expression by nearly ninefold (p &lt; 0.05). All these effects were prevented when identical experiments were carried out in the presence of TTX, but the expression of NHE-1. The expression of sodium channel protein type 5 subunit alpha was unaffected by either ISO or TTX. When taken together, these studies show that TTX attenuates the hypertrophic effect of ISO and suggest a possible approach to limiting ISO-induced hypertrophy in clinical treatment. 

Retracted: No

PubPeer comments:
 Figures 5A and 5D. * Red boxes: One of the SCN5A lanes looks like a NKA-a3 lane. Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. ![file] ,
MicroRNA‑199a‑5p regulates FOXC2 to control human vascular smooth muscle cell phenotypic switch
Authors: Yushi Cao
Weitie Wang
Lei Li
Xiangyu Jie
Zhongwen Cao
Journal: Molecular Medicine Reports (2021)
Discipline: CLINICAL MEDICINE
Keywords: FOXC2; VSMCs; miRNA‑199a‑5p; varicose veins.
Affiliations: Department of Hepatobiliary Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Vascular Surgery, Qianwei Hospital of Jilin Province, Changchun, Jilin 130012, P.R. China., Department of Cardiovascular Surgery, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.

Abstract:  Varicose veins are among the most common disorders of the vascular system; however, the pathogenesis of varicose veins remains unclear. The present study aimed to investigate the roles of microRNA (miR)‑199a‑5p in varicose veins and in the phenotypic transition of vascular smooth muscle cells (VSMCs). Bioinformatics analysis confirmed that miR‑199a‑5p had target sites on the forkhead box C2 (FOXC2) 3'‑untranslated region. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting were used to detect the expression levels of miR‑199a‑5p and FOXC2 in varicose vein and normal great saphenous vein tissues. Cell Counting Kit‑8 and Transwell migration assays were performed to validate the effects of miR‑199a‑5p on VSMCs. Contractile markers, such as smooth muscle 22α, calponin, smooth muscle actin and myosin heavy chain 11 were used to detect phenotypic transition. RT‑qPCR revealed that miR‑199a‑5p was downregulated in varicose veins compared with expression in normal great saphenous veins, whereas FOXC2 was upregulated in varicose veins. In addition, biomarkers of the VSMC contractile phenotype were downregulated in varicose veins. Overexpression of miR‑199a‑5p by mimics suppressed VSMC proliferation and migration, whereas depletion of miR‑199a‑5p enhanced VSMC proliferation and migration. Notably, the effects caused by miR‑199a‑5p could be reversed by FOXC2 overexpression. Dual luciferase reporter analysis confirmed that FOXC2 was a target of miR‑199a‑5p. In conclusion, miR‑199a‑5p may be a novel regulator of phenotypic switching in VSMCs by targeting FOXC2 during varicose vein formation. 

Retracted: No

PubPeer comments:
 Figure 2. I suggest that the authors check the original files to make sure they did not put the picture upside down. ![file] ,
Dicer reprograms stromal fibroblasts to a pro-inflammatory and tumor-promoting phenotype in ovarian cancer
Authors: Xiao Wei
Qinglei Gao
Sen Xu
Ping Jin
Gang Chen
Xin Yang
Taoran Zhang
Ding Ma
Chaoyang Sun
Zongyuan Yang
Xiaoting Li
Journal: Cancer Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: Dicer; Inflammation; Ovarian cancer; Reprogram; Stromal fibroblast.
Affiliations: Cancer Biology Research Center, Key Laboratory of the Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China., Cancer Biology Research Center, Key Laboratory of the Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China. Electronic address: .

Abstract:  Inflammation and host stromal activation contribute significantly to ovarian cancer (OC) initiation and malignant progression. However, the complex reciprocal interactions between them are largely unknown. Here, we discovered that the tumor suppressor gene Dicer was paradoxically overexpressed in ovarian tumor stroma, and induced fibroblast activation and stromal inflammation. Dicer transformed normal fibroblasts to a carcinoma-associated fibroblast (CAF)-like state, which was morphologically spread out and functionally activated to fuel tumor invasion and metastasis. Attenuation of Dicer hampered CAF characteristics, diminished stromal inflammation and the role of fibroblasts in supporting tumor growth. Moreover, Dicer drove the expression of an "inflammatory signature" in fibroblasts that could be used to discriminate normal and cancerous stroma and predict the survival of patients with OC. Finally, the nuclear factor κ B (NFκB) signaling was demonstrated to be responsible for Dicer effect on fibroblast activation and stromal inflammation, through microRNA (miR)-6780b. Our study represents the first report that characterizes Dicer expression and function in the tumor stroma, and highlights its pro-metastatic role in this context. Additionally, we suggest that the Dicer-miR6780b-NFκB cascade is an attractive target of choice in stroma-oriented OC therapy. 

Retracted: No

PubPeer comments:
 Figure 4e in Reprogramming of stromal fibroblasts by SNAI2 contributes to tumor desmoplasia and ovarian cancer progression Molecular Cancer (2017) - 0 Comments pubmed: 29041931 doi: 10.1186 s12943-017-0732-6 issn: 1476-4598 Figure 3B in Dicer reprograms stromal fibroblasts to a pro-inflammatory and tumor-promoting phenotype in ovarian cancer Cancer letters (2018) - 0 Comments pubmed: 29199004 doi: 10.1016 j.canlet.2017.11.026 issn: 1872-7980 issn: 0304-3835 ![file] , 
 Corrigendum, [28 January 2020:] :  The authors would like to correct Figure 3, as the representative 3D organotypic image in Fig. 3B (Dicer1-KO group) was errorly used in the preparation of figure for publication. We sincerely apologize for having this error in the article, and apologize for any inconvenience caused. The authors have provided corrected version of Figure 3 here. ![] ,
Vitamin D increases the production of IL-10 by regulatory T cells in patients with systemic sclerosis
Authors: Giuliana Guggino
Concetta Scazzone
Marianna Lo Pizzo
Francesco Ciccia
Francesco Dieli
Guido Sireci
Paola Cipriani
Roberto Giacomelli
Luisa Agnello
Piero Ruscitti
Diana Di Liberto
Gaetano La Rocca
Marcello Ciaccio
Giovanni Triolo
Journal: Clinical and experimental rheumatology (0)
Discipline: CLINICAL MEDICINE
Keywords: Vitamin D; autoimmune diseases; regulatory T cells; Tregs; systemic sclerosis
Affiliations: Dipartimento di Biopatologia e Biotecnologie Mediche, University of Palermo, Italy., Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, University of Palermo, Italy., Division of Rheumatology, Department of Biotechnological and Applied Clinical Science, School of Medicine, Università dell' Aquila, Italy., Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, University of Palermo, Italy. .

Abstract:  Objectives: Vitamin D status influences the risk to develop autoimmune diseases affecting the percentage and/or functions of regulatory T cells (Tregs). Since low levels of 25 (OH) D have been decreased in patients with systemic sclerosis (SSc), we aimed to study the effect of Vitamin D3 (cholecalciferol) supplementation on Tregs frequencies and functions. Methods: Peripheral blood and sera samples were obtained from 45 SSc patients and controls (HC). A number of eighteen SSc patients had consumed Cholecalciferol (orally) at the dose of 25.000 UI/month for 6 months at the time of enrollment. 25(OH)D serum levels were measured and VDR polymorphisms, were genotyped by polymerase chain reaction (PCR). Tregs isolated from peripheral blood mononuclear cells were in vitro expanded and a suppression assay was performed. Flow cytometry analysis was then carried out. Finally, IL-10 production was assayed by ELISA. Results: Low serum levels of 25(OH)D were detected in SSc patients. The percentage of Tregs in SSc patients was similar to controls, but, among SSc patients, it was higher in those patients taking cholecalciferol. Tregs capability to suppress T cell proliferation was impaired in SSc patients and not restored after in vitro pre-treatment with the active form of Vitamin D (1,25(OH)2D3); but at the same time the production of IL-10 was increased in treated samples obtained from patients. The lack of response of Tregs from SSc patients to 1,25(OH)2D3 treatment in vitro was not due to altered Vitamin D/VDR signalling. Conclusions: Altogether, our results indicate that the increased production of IL-10 by 1,25(OH)2D3 -treated Tregs could provide a "suppressive" cytokine milieu able to modulate immune response but it is not sufficient to restore the immune suppressive functions of Tregs. 

Retracted: No

PubPeer comments:
 There are some odd duplicated areas between panels in Figure 1 and 2 ![file] ,
Simultaneous Determination of Fluoride and Chloride in Iron Ore by Steam Distillation Followed by Ion Chromatography
Authors: Muhammad, Nadeem
Lao, Lehua
Intisar, Azeem
Cui, Hairong
Zhu, Yan
Journal: Chromatographia (2019)
Discipline: CHEMISTRY
Keywords: extraction; fluoride; chloride; inorganic iron ore; steam distillation

Abstract: This study illustrates the extraction of fluoride (F\u2212) and chloride (Cl\u2212) from non-combustible inorganic iron ore matrix by employing steam distillation (SD)-based volatilization process followed by ion chromatographic (IC) determination. This cost-effective, simple and green sample preparation setup involved decomposition of sample matrix in H2SO4 for the extraction of volatile halides at 165–180&nbsp;°C that were subsequently collected in a 100-mL receiving bottle having 0.2&nbsp;M NaOH as absorption solution. After 15–20&nbsp;min of absorption, the distillate was injected to the IC system for the isocratic separation and determination of both halides in complex inorganic iron ore sample (IOS). The developed method showed good linearity in the concentration range of 0.02–10&nbsp;\xb5g/mL with a correlation coefficient (R) greater than\u2009≥\u20090.9999. It also showed good accuracy (82.20–87.87%), precision (RSDs\u2009≤\u20093.71) and excellent limit of detection (LOD) ranged between 0.0003 and 0.0006&nbsp;\xb5g/mL with no matrix effect.

Retracted: No

PubPeer comments:
 The paper describes a steam distillation procedure for F and Cl separation followed by ion chromatographic determination. On reading the paper I found that the data are unreal and some of the points which lead to this conclusion are listed below. (1) The LODs mentioned in table 1, for F determination (0.0003 and 0.0006 u03bcg mL) are unreal and can not be achieved using the ion chromatography procedure followed by the authors. (2)The F and Cl recovery studies were carried out with a reference material numbered 1811000321 and as per the graphs presented in the fig 2 F recovery is always higher than that of Cl. In the the table 2 the F and Cl values and their recoveries for 1811000321 are tabulated. Now we can see that in the table F recovery is much lower (83.33%) as compared to Cl (93.05%). (3) The authors have reported that 0.5 g of sample was distilled and final distillate volume was 90-95 mL. If we consider the certified F values from table -2, lets say 0.552 u03bcg mL (don t know why concentration in a solid is reported per mL), the distillate will have F concentration around 0.003 u03bcg mL. In table the concentration range for ion chromatography analysis is reported (0.02-10 u03bcg mL), where the lowest limit is 10 times higher than the F concentration in the distillate. The question is then how the samples were analysed. Based on these points, I want to report here that the methods described by N. Muhammad and et. al. in Chromatographia paper (doi.org 10.1007 s10337-019-03798-7) is based upon unreal informations and results and can not be reproduced. I doubt the data are false and fabricated. ![file] ![file] ![file] ![file] ,
Long intergenic non-protein coding RNA 00475 silencing acts as a tumor suppressor in glioma under hypoxic condition by impairing microRNA-449b-5p-dependent AGAP2 up-regulation
Authors: Xiaoyu Qiu
Lei Yu
Xi&#x27;an Zhang
Jun Fan
Si Gui
Binghui Qiu
Jun Pan
Songtao Qi
Guozhong Zhang
Yawei Liu
Journal: Therapeutic Advances in Medical Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: AGAP2; LINC00475; glioma; hypoxia; invasion
Affiliations: Department of Neurosurgery, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou 510515, Guangdong Province, P. R. China, Department of Radiology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, P. R. China, Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, P. R. China

Abstract:  Objective: Long non-coding RNAs have been demonstrated to be involved in the progression of a variety of cancers, including glioma. Through microarray analyses, long intergenic non-protein coding RNA 00475 (LINC00475) was identified in the glioma development. However, its potential role remains incompletely understood. This study aimed to elucidate the effect of LINC00475 on the development of glioma under hypoxic conditions. Methods: Glioma cells underwent hypoxic treatment and were collected. The functional role of LINC00475 and AGAP2 in glioma was determined using ectopic expression, depletion, and reporter assay experiments. Then, the expression of LINC00475, microRNA (miR)-449b-5p, AGAP2, FAK, and HIF-1α was determined. In addition, cell migration and invasion were examined. Finally, a tumor xenograft was carried out in nude mice to explore the role of LINC00475 on oxidation in vivo. Results: LINC00475 was identified to be overexpressed in hypoxic glioma samples, which was further observed to bind to and down-regulate miR-449b-5p, and negatively targeted AGAP2. Moreover, we also revealed a positive correlation between LINC00475 and AGAP2 expression in glioma. In addition, silencing of LINC00475 decreased the extent of FAK phosphorylation and reduced the expression of HIF-1α and AGAP2. It was also observed that LINC00475 silencing suppressed glioma cell proliferation, migration, and invasion, and promoted cell apoptosis. Moreover, oxidation of nude mice was promoted by LINC00475 silencing. Conclusion: Taken together, LINC00475 silencing exerted an inhibitory effect on glioma under hypoxic conditions by down-regulating AGAP2 via up-regulation of miR-449b-5p. 

Retracted: No

PubPeer comments:
 Figs 2D, 4B, 4G, 5F. These are curiously stylised Western Blots, devoid of background. The protein blobs maintain the same string-of-sausages morphology between gels, and (within gels), between bands, as the proteins migrate across each gel. Is it possible for the authors to upload or link to scans of the original gels? ![file] Similar WBs appear elsewhere in the literature (sometimes in papers that [were retracted] for being products of a papermill). Here is a montage I prepared earlier: ![] ,
Fluorescence-phosphorescence dual emissive carbon nitride quantum dots show 25% white emission efficiency enabling single-component WLEDs
Authors: Fanglong Yuan
Xiaohong Li
Louzhen Fan
Ting Yuan
Yunchao Li
Shihe Yang
Journal: Chemical science (2019)
Discipline: CHEMISTRY
Keywords: white light-emitting diodes; W-CNQDs; quantum efficiency; singlet; triplet states
Affiliations: College of Chemistry , Beijing Normal University , Beijing , 100875 , China . Email: ., Guangdong Key Lab of Nano-Micro Material Research , School of Chemical Biology and Biotechnology , Shenzhen Graduate School , Peking University , Shenzhen 518055 , China . Email: .

Abstract:  Developing efficient single-component white light-emitting diodes (WLEDs) is extremely challenging due to the issue of Kasha's rule. Here we report the first demonstration of blue-yellow fluorescence-phosphorescence dual emission from our newly minted single-component white emissive carbon nitride quantum dots (W-CNQDs). The W-CNQDs deliver an overall photoluminescence quantum efficiency of 25%, which is the highest value among white-emitting materials reported to date, based on utilizing both singlet and triplet states. Experimental and theoretical investigations reveal that the carbonyl groups at the rim of the W-CNQDs play a key role in promoting intersystem crossing and inducing intermolecular electronic coupling, affording intensive yellow phosphorescence. Efficient white emission is achieved with a phosphorescence quantum efficiency of 6% under ambient conditions. A WLED is fabricated by integrating W-CNQD phosphors into a UV-LED chip, which shows favorable white light characteristics with CIE coordinates and a CRI of (0.35, 0.39) and 85, respectively, demonstrating good color chromatic stability. This work opens up new opportunities for exploring dual emission mechanisms and designs to facilitate the development of efficient single-component WLEDs. 

Retracted: No

PubPeer comments:
 Unexpected similarity between fragments of solid 13C NMR spectrum of W-CNQDs (Figure 2) and B-CNQDs (Figure S22). ![file] , 
 Comparing Fig. 2(b)  a TEM image of the W-CNQDs after ultrasonic dispersion in water with Supplementary Fig Figure S19(a)  TEM image of the B-CNQDs after ultrasonic dispersion in water . ![file] Different materials, different background textures, but the spacing of the QDs is more similar than I would expect. , 
 #2 a) looks like a higher magnification image of the region in b). The diffraction conditions have changed a bit, that is likely why the particle in the middle looks darker in a) vs b). Judging by the contamination build-up, a) was taken before b). who knows where the fringey inset images come from. ,
Mss4 gene is up-regulated in rat brain after chronic treatment with antidepressant and down-regulated when rats are anhedonic
Authors: Dominique Aunis
Claude Muller
Michel Maitre
Michael Spedding
Catherine Schmidt-Mutter
Christian Andriamampandry
Serge Gobaille
Journal: Molecular Pharmacology (2002)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Differential display; reverse transcription-polymerase chain reaction; mRNA; tricyclic antidepressant; imipramine
Affiliations: Institut de Chimie Biologique, U-338, Faculty of Medicine, Strasbourg, France.

Abstract:  Differential display reverse transcription-polymerase chain reaction was used to identify mRNAs that are differentially expressed in the brain of rats treated chronically with the reference tricyclic antidepressant, imipramine, in comparison with control rats. The gene encoding for a mutation suppressor for Sec4-8 yeast (Mss4) transcript is overexpressed in the amygdala of treated rats after 3 weeks of daily administration. This overexpression is also found in the hippocampus of rats treated chronically with either tianeptine or fluoxetine. Mss4 protein has the properties of a guanine nucleotide exchange factor, interacting with several members of the Rab family implicated in Ca(2+)-dependent exocytosis of neurotransmitters. Mss4 was also overexpressed in other brain structures as judged by in situ hybridization. The kinetics of the up-regulation of Mss4 gene expression measured by Northern blot during the imipramine, tianeptine, or fluoxetine treatments are consistent with an antidepressant effect that occurs after 3 weeks. In rats in which anhedonia was induced by chronic mild stress during 3 weeks, Mss4 transcripts were specifically down-regulated in hippocampus and amygdala compared with control rats. It is proposed that Mss4 protein, which stimulates exocytosis in vivo, participates in the potentiation of the activity of neurotransmitter pathways implicated in the action of several antidepressants and constitutes one of the common functional molecules induced after chronic antidepressant treatment. 

Retracted: No

PubPeer comments:
 There are multiple duplications (in images 3, 4 7) where blots are too similar than could ever be expected by chance. This extends also to the random noise in the background. Some examples below. Figure 3. ![file] Figure 4. Note the added artifacts in green. ![file] Figure 7. ![file] Perhaps the authors can explain? Maybe they have saved higher resolution scans? ,
Coeliac disease: a histological follow-up study
Authors: C Di Bella
P Velio
G Casella
B M Cesana
A Lanzini
M Gambarotti
M T Bardella
G Bassotti
L Prampolini
V Villanacci
Journal: Histopathology (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: histological response; gluten-free diet; coeliac patients; mucosal damage; clinical remission
Affiliations: Department of Gastroenterology and Endocrine Diseases, Fondazione IRCCS, Ospedale Maggiore Policlinico, Mangialli and Regina Elena, Milano, Italy. 

Abstract:  Aims: To assess the histological response to a gluten-free diet (GFD) in a series of coeliac patients in clinical remission, of different ages and with varying degrees of mucosal damage at diagnosis. Methods and results: Biopsy samples from 249 coeliac patients (F 165, M 84) were analysed basally and after clinical and biochemical remission following a GFD. All patients showed an improvement in mucosal findings after starting a GFD, but complete histological normalization was observed in 74.1% of paediatric cases (diagnosed before 14 years of age) and in only 17.5% of adults. Statistical analysis showed that sex, the clinical picture at diagnosis and the length of time between biopsy at the time of diagnosis and on a GFD were not related to histological normalization. In contrast, the age at diagnosis was statistically significantly related to it (P &lt; 0.0001). In addition, the presence/absence of Helicobacter pylori was independent of the normalization of the duodenal mucosa. Conclusions: In clinical practice the criteria for diagnosis of coeliac disease are sufficiently standardized, whereas for follow-up they are less well defined. We suggest that in order to compare the results from different studies, it should be stated whether remission after treatment is based on clinical or histological criteria or both. 

Retracted: No

PubPeer comments:
 The same histology in these two papers refers to a patient from Italy (left) and to a patient from Iran (right). the later in the context of H.pylory infection. Which one is correct? ![file] , 
 More duplications ![file] , 
 Figure 1. Image duplications in three papers by the same of authors (Bassotti G and Villanacci V). In addition to plagiarism, in contrast to the figure s legend, the images shown in Figure 1A and B are from two different patients. Could the authors comment on that.? ![file] , 
 ![file] ,