PReD-Bench/PRed-Bench huggingface dataset:
Development and functional characterization of insulin-releasing human pancreatic beta cell lines produced by electrofusion
Authors: Muhajir Hamid
Peter R Flatt
Jane T McCluskey
Hong Guo-Parke
Ramon Gomis
Neville H McClenaghan
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: insulin-releasing cell lines; electrofusion; pancreatic beta cells; PANC-1 epithelial cell line; insulin secretion
Affiliations: SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine BT52 1SA, Northern Ireland, United Kingdom. 

Abstract:  Three novel human insulin-releasing cell lines designated 1.1B4, 1.4E7, and 1.1E7 were generated by electrofusion of freshly isolated of human pancreatic beta cells and the immortal human PANC-1 epithelial cell line. Functional studies demonstrated glucose sensitivity and responsiveness to known modulators of insulin secretion. Western blot, RT-PCR, and immunohistochemistry showed expression of the major genes involved in proinsulin processing and the pancreatic beta cell stimulus-secretion pathway including PC1/3, PC2, GLUT-1, glucokinase, and K-ATP channel complex (Sur1 and Kir6.2) and the voltage-dependent L-type Ca(2+) channel. The cells stained positively for insulin, and 1.1B4 cells were used to demonstrate specific staining for insulin, C-peptide, and proinsulin together with insulin secretory granules by electron microscopy. Analysis of metabolic function indicated intact mechanisms for glucose uptake, oxidation/utilization, and phosphorylation by glucokinase. Glucose, alanine, and depolarizing concentrations of K(+) were all able to increase [Ca(2+)](i) in at least two of the cell lines tested. Insulin secretion was also modulated by other nutrients, hormones, and drugs acting as stimulators or inhibitors in normal beta cells. Subscapular implantation of the 1.1B4 cell line improved hyperglycemia and resulted in glucose lowering in streptozotocin-diabetic SCID mice. These novel human electrofusion-derived beta cell lines therefore exhibit stable characteristics reminiscent of normal pancreatic beta cells, thereby providing an unlimited source of human insulin-producing cells for basic biochemical studies and pharmacological drug testing plus proof of concept for cellular insulin replacement therapy. 

Retracted: No

PubPeer comments:
  ,
Monodisperse thiourea functionalized graphene oxide-based PtRu nanocatalysts for alcohol oxidation
Authors: Hakan Burhan
Esra Kuyuldar
Sibel Demiroglu Mustafov
Aysegul Iyidogan
Fatih Sen
Su Selda Polat
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Thiourea; Graphene oxide; PtRu nanocatalysts; Methanol oxidation reactions; Functionalization
Affiliations: Sen Research Group, Department of Biochemistry, Faculty of Arts and Science, Dumlupƒ±nar University, Evliya √áelebi Campus, 43100, K√ºtahya, Turkey., Department of Chemistry, Faculty of Science and Arts, Gaziantep University, Gaziantep, Turkey., Sen Research Group, Department of Biochemistry, Faculty of Arts and Science, Dumlupƒ±nar University, Evliya √áelebi Campus, 43100, K√ºtahya, Turkey. .

Abstract:  Addressed herein, thiourea functionalized graphene oxide-based PtRu nanocatalysts (PtRu@T/GO) has been synthesized and characterized by several techniques and performed for methanol oxidation reactions as novel catalysts. In this study, graphene oxide (GO) was functionalized with thiourea (T/GO) in order to obtain monothiol functionalized graphene and increase the stability and activity of the nanocatalysts. Raman spectroscopy, X-ray photoelectron spectroscopy (XPS), X-ray diffraction (XRD), TEM (transmission electron microscopy) and high-resolution transmission electron microscopy (HR-TEM) were used for characterization of the prepared nanocatalysts. The results obtained from these techniques showed that the prepared nanocatalysts were in a highly crystalline form, well dispersed on T/GO, very small in size and colloidally stable. The average size of the synthesized nanocatalysts determined by TEM analysis was found to be 3.86 ¬± 0.59 nm. With HR-TEM analysis, the atomic lattice fringes of the nanocatalysts were calculated to be 0.23 nm. After the full characterization of the prepared nanocatalysts, they were tried for the methanol oxidation reaction (MOR) and it was observed that 97.3% of the initial performance was maintained even after 1000 cycles while exhibiting great catalytic activity and stability with the help of T/GO. Thus, the arranged nanocatalysts displayed great heterogeneous catalyst characteristics for the methanol oxidation response. 

Retracted: No

PubPeer comments:
 Inset of Figure 2: X-ray diffraction pattern of as-prepared Pt@T GO and PtRu@T GO nanocatalysts. Two copies of the same pattern:  , 
 Inset with ETM image of nanoparticle is Type I. Identified by Elisabeth Bik in +30 papers:  https: pubpeer.com publications 8AD71F4A32472314CCE9983D47E36F Type 1 histogram found in many papers in variety of designs, different x-scale (size of particles) and the same relative height of bars.  see for example 5 copies here: https: pubpeer.com publications F5517C2786C02B2C34E63266AC642A One more here: https: pubpeer.com publications 8AD71F4A32472314CCE9983D47E36F Earliest so far found in 2016 paper https: doi.org 10.1039 C6RA13142E I hope somebody could make full list for papers which include this histogram (possibly many more to be found) ,
Determination of Serum Lost Goodwill Target Proteome in Patients with Severe Traumatic Brain Injury
Authors: Jinrui Ren
Hongchao Liu
Hongming Ji
Dongsheng Guo
Junwen Wang
Jun Li
Wenxiao Sun
Ruifan Xie
Changchen Hu
Gangli Zhang
Yihu Tan
Zhipeng Hao
Journal: BioMed Research International (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: biokinetics; LGT proteome; biomarker; severe TBI; serum
Affiliations: Department of Neurosurgery, Shanxi Provincial People's Hospital, Taiyuan 030001, China., Department of Neurosurgery, Shanxi Provincial People's Hospital, Taiyuan 030001, China ; Department of Neurosurgery, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China., Department of Neurosurgery, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430077, China., Department of Neurosurgery, Wuhan Central Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China., Department of Neurosurgery, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Abstract:  This study investigates the biokinetics of LGT proteome, a potential biomarker of severe TBI, in serum of severe TBI patients. The LGT proteome presents in the serum of severe TBI patients. The abundance diversity of LGT proteome is closely associated with pathologic condition of TBI patients. Serum LGT proteome may be used as a promising marker for evaluating severity of severe TBI. 

Retracted: No

PubPeer comments:
 In the article titled u201cDetermination of Serum Lost Goodwill Target Proteome in Patients with Severe Traumatic Brain Injuryu201d [1], there was an incomplete description of how the results related to our earlier publications. The predictive value of LGT in TBI was also overestimated. We apologise for this and explain below the relationship between our articles, why we classified the patients as we did, and the use of the grants for this research. Rather lengthy correction in full: https: doi.org 10.1155 2018 5234910 ,
Bazhen decoction protects against acetaminophen induced acute liver injury by inhibiting oxidative stress, inflammation and apoptosis in mice
Authors: Erqun Song
Juanli Fu
Xiaomin Xia
Chuanyang Su
Yang Song
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Bazhen decoction; anti-oxidative; anti-inflammatory; anti-apoptosis; acetaminophen
Affiliations: Key Laboratory of Luminescence and Real-Time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University, Chongqing, People's Republic of China.

Abstract:  Bazhen decoction is a widely used traditional Chinese medicinal decoction, but the scientific validation of its therapeutic potential is lacking. The objective of this study was to investigate corresponding anti-oxidative, anti-inflammatory and anti-apoptosis activities of Bazhen decoction, using acetaminophen-treated mice as a model system. A total of 48 mice were divided into four groups. Group I, negative control, treated with vehicle only. Group II, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days. Group III, received a single dose of 900 mg/kg acetaminophen. Group IV, fed with 500 mg/kg/day Bazhen decoction for 10 continuous days and a single dose of 900 mg/kg acetaminophen 30 min before last Bazhen decoction administration. Bazhen decoction administration significantly decrease acetaminophen-induced serum ALT, AST, ALP, LDH, TNF-Œ±, IL-1Œ≤, ROS, TBARS and protein carbonyl group levels, as well as GSH depletion and loss of MMP. Bazhen decoction restore SOD, CAT, GR and GPx activities and depress the expression of pro-inflammatory factors, such as iNOS, COX-2, TNF-Œ±, NF-Œ∫B, IL-1Œ≤ and IL-6, respectively. Moreover, Bazhen decoction down-regulate acetaminophen-induced Bax/Bcl-2 ratio, caspase 3, caspase 8 and caspase 9. These results suggest the anti-oxidative, anti-inflammatory and anti-apoptosis properties of Bazhen decoction towards acetaminophen-induced liver injury in mice. 

Retracted: No

PubPeer comments:
 Much more similar than expected  , 
 Green box: unnatural band Yellow box: similar bands  , 
 Much more similar than expected.  , 
 Much more similar than expected.  , 
 Much more similar than expected!  , 
 Much more similar than expected.  , 
  ,
Resveratrol Supplementation Attenuates Cognitive and Molecular Alterations under Maternal High-Fat Diet Intake: Epigenetic Inheritance over Generations
Authors: Christian Gri√±√°n-Ferr√©
Merc√® Pall√†s
Ver√≥nica Palomera-√Åvalos
Vanesa Izquierdo
Journal: International Journal of Molecular Sciences (2021)
Discipline: CHEMISTRY
Keywords: -Methyladenosine methylation; /sup&gt; 6&lt; N&lt; SAMP8
Affiliations: Department of Pharmacology and Therapeutic Chemistry, Institut de Neuroci√®ncies-Universitat de Barcelona, Avda. Joan XXIII, 27., 08028 Barcelona, Spain., Department of Cellular and Molecular Biology, University Center of Biological and Agricultural Sciences, University of Guadalajara, km 15.5 Guadalajara-Nogales Highway, Zapopan 45110, Jalisco, Mexico.

Abstract:  Environmental factors such as maternal high-fat diet (HFD) intake can increase the risk of age-related cognitive decline in adult offspring. Epigenetic mechanisms are a possible link between diet effect and neurodegeneration across generations. Here, we found a significant decrease in triglyceride levels in a high-fat diet with resveratrol (RSV) HFD + RSV group and the offspring. Firstly, we obtained better cognitive performance in HFD+RSV groups and their offspring. Molecularly, a significant increase in DNA methylation (5-mC) levels, as well as increased gene expression of DNA methyltransferase 1 (Dnmt1) and Dnmt3a in HFD + RSV F1 group, were found. Furthermore, a significant increase of N6-Methyladenosine methylation (m6A) levels in HFD+RSV F1, as well as changes in gene expression of its enzymes Methyltransferase like 3 (Mettl3) and FTO alpha-ketoglutarate dependent dioxygenase (Fto) were found. Moreover, we found a decrease in gene expression levels of pro-inflammatory markers such as Interleukin 1Œ≤ (Il1-Œ≤), Interleukin 6 (Il-6), Tumor necrosis factor-Œ± (Tnf-Œ±), C-X-C motif chemokine ligand 10 (Cxcl-10), the pro-inflammatory factors monocyte chemoattractant protein 1 (Mcp-1) and Tumor growth factor-Œ≤1 (Tgf-Œ≤1) in HFD+RSV and HFD+RSV F1 groups. Moreover, there was increased gene expression of neurotrophins such as Neural growth factor (Ngf), Neurotrophin-3 (Nt3), and its receptors Tropomyosin receptor kinase TrkA and TrkB. Likewise, an increase in protein levels of brain-derived neurotrophic factor (BDNF) and phospho-protein kinase B (p-Akt) in HFD+RSV F1 was found. These results suggest that maternal RSV supplementation under HFD intake prevents cognitive decline in senescence-accelerated mice prone 8 (SAMP8) adult offspring, promoting a reduction in triglycerides and leptin plasma levels, changes in the pro-inflammatory profile, and restoring the epigenetic landscape as well as synaptic plasticity. 

Retracted: No

PubPeer comments:
 Dear Sir, I appreciate your excellent work on retraction watch and I am one of the regular readers of this. Did you notice the images in this article? Figure 2. (A) Figure 6. (B) of Western blot and confocal microscopy images. Figure 3 4. (B) of Western blot and confocal microscopy images: CDR1 ,
Colonic flora, probiotics, obesity and diabetes
Authors: Paul E Marik
Journal: Frontiers in Endocrinology (2012)
Discipline: CLINICAL MEDICINE
Keywords: obesity and diabetes; probiotics.
Affiliations: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Eastern Virginia Medical School, Norfolk, VA, USA.

Abstract:  Obesity results from alterations in the body's regulation of energy intake, expenditure, and storage. Animal and human data demonstrate that phylogenic changes occur in the microbiota composition in obese individuals. Furthermore, evidence from animal models suggest that the alterations of the gut microbiota with obesity results in increased energy extraction and lipid deposition, altered release of entero-hormones, increased intestinal permeability and metabolic endotoxemia. Treatment with pre- and probiotics may reverse many of metabolic effects linked with the altered microbiota in obese patients. The gut microbiota is, therefore, a potential nutritional and pharmacological target for the management of obesity and obesity-related disorders. 

Retracted: No

PubPeer comments:
 This paper has been retracted in August 2013. The retraction notice can be found here: https: www.frontiersin.org articles 10.3389 fendo.2013.00110 full It reads: * The corresponding author (Paul E. Marik) and the journal wish to retract the 11 July 2012 article cited above. While all parties are convinced of the value of this work, this Mini Review was found to contain text that was improperly cited. We regret this inconvenience and apologize to the readers of Frontiers in Endocrinology.* Perhaps  found to contain text is a bit understated. Here is the complete text, with text marked in color identical to text from older papers. Each color stands for a different source paper. At least 10 source papers appear to have been used.  ,
Binding of p190RhoGEF to a destabilizing element on the light neurofilament mRNA is competed by BC1 RNA
Authors: Hong Lin
Zhenying Nie
Jinbin Zhai
Weiwen Ge
Junhua Wu
William W Schlaepfer
Rafaela Canete-Soler
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RNA-mediated motor neuron degeneration; transgenic mice; mRNA instability determinant; neurofilament (NF-L) transgene; RNA binding factors
Affiliations: Division of Neuropathology, University of Pennsylvania Medical School, Philadelphia, Pennsylvania 19104-6100, USA.

Abstract:  The enhancement of RNA-mediated motor neuron degeneration in transgenic mice by mutating a major mRNA instability determinant in a light neurofilament (NF-L) transgene implicates cognate RNA binding factors in the pathogenesis of motor neuron degeneration. p190RhoGEF is a neuron-enriched guanine exchange factor (GEF) that binds to the NF-L-destabilizing element, to c-Jun N-terminal kinase-interactive protein-1 (JIP-1), and to 14-3-3 and may link neurofilament expression to pathways affecting neuronal homeostasis. This study was undertaken to identify additional RNA species that bind p190RhoGEF and could affect interactions of the exchange factor with NF-L transcripts. The C-terminal domain of p190RhoGEF, containing the RNA-binding site, was expressed as a glutathione S-transferase fusion protein and was used as an affinity probe to isolate interactive RNAs in rat brain extracts. As expected, NF-L mRNA was identified as an RNA specie eluted from the affinity column. In addition, BC1 RNA was also found enriched in the bound RNA fraction. BC1 is a 152-nucleotide RNA that is highly expressed but untranslated in differentiated neurons. We show that BC1 and NF-L mRNA bind to a similar site in the C-terminal domain of p190RhoGEF, and their bindings to p190RhoGEF are readily cross-competed. Moreover, we identify a novel binding site in BC1 to account for its interaction with p190RhoGEF. The findings suggest a novel role of BC1 in differentiated neurons involving RNA-protein interactions of p190RhoGEF. 

Retracted: No

PubPeer comments:
 Figure 5. Much more similar than you would expect. https: imgur.com By4PZDs , 
 #1 Figure 5. Left hand half band lane M3 figure 5C and left hand half band lane  full figure 5D. Much more similar than you would expect. https: imgur.com eCNqqSj ,
Modularity of the oncoprotein-like properties of platelet glycoprotein Ibalpha
Authors: Youjun Li
Jie Lu
Edward V Prochownik
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glycoprotein Ib alpha; von Willebrand factor receptor; c-Myc oncoprotein; megakaryocytes; platelets
Affiliations: Section of Hematology/Oncology, Children's Hospital of Pittsburgh Pittsburgh, Pennsylvania 15213, USA.

Abstract:  Glycoprotein Ib alpha (GpIbalpha), a trans-membrane glycoprotein, is expressed on the surface of megakaryocytes and platelets, where, in association with glycoprotein Ib beta, glycoprotein V, and glycoprotein IX, it normally forms the von Willebrand factor receptor (vWFR). A fully functional vWFR is necessary for platelet attachment, aggregation, and activation and has also been shown to regulate megakaryocyte ploidy. We have recently shown that the gene encoding GpIbalpha is a transcriptional target for the c-Myc oncoprotein and is more widely expressed than previously thought, with particularly high levels occurring in transformed cells. Indeed, GpIbalpha can substitute for c-Myc in promoting growth, transformation, and genomic instability. In the current work, we have demonstrated that, despite the promiscuous expression of GpIbalpha, other vWFR subunits remain largely restricted to megakaryocytes. We have characterized a panel of GpIbalpha mutants and shown that some regions of the protein essential for vWFR activity are not necessary for c-Myc-like functions. Specifically, the six C-terminal amino acids of the cytoplasmic domain, which mediate vWFR signaling, are entirely dispensible for the c-Myc-like functions of GpIbalpha. Instead, these require a more membrane-proximal filamin-binding domain. Also important is the GpIbalpha signal peptide, which, in the absence of other vWFR subunits, directs GpIbalpha to the endoplasmic reticulum rather than the membrane. Together, these results provide strong evidence that the domains of GpIbalpha mediating c-Myc-like functions are modular, genetically distinct, and independent of those involved in vWFR signaling. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected. https: imgur.com LMzT4t9 , 
 Figure 3. Much more similar than expected. https: imgur.com ttFBFDD ,
Context-dependent function of regulatory elements and a switch in chromatin occupancy between GATA3 and GATA2 regulate Gata2 transcription during trophoblast differentiation
Authors: M A Karim Rumi
Soumen Paul
Debasree Dutta
Soma Ray
Michael J Soares
Lindsey N Kent
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: GATA transcription factors; tissue-specific gene expression; GATA2; GATA3; trophoblast-specific genes
Affiliations: Institute of Maternal-Fetal Biology and the Division of Cancer & Developmental Biology, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.

Abstract:  GATA transcription factors are important regulators of tissue-specific gene expression during development. GATA2 and GATA3 have been implicated in the regulation of trophoblast-specific genes. However, the regulatory mechanisms of GATA2 expression in trophoblast cells are poorly understood. In this study, we demonstrate that Gata2 is transcriptionally induced during trophoblast giant cell-specific differentiation. Transcriptional induction is associated with displacement of GATA3-dependent nucleoprotein complexes by GATA2-dependent nucleoprotein complexes at two regulatory regions, the -3.9- and +9.5-kb regions, of the mouse Gata2 locus. Analyses with reporter genes showed that, in trophoblast cells, -3.9- and +9.5-kb regions function as transcriptional enhancers in GATA motif independent and dependent fashions, respectively. We also found that knockdown of GATA3 by RNA interference induces GATA2 in undifferentiated trophoblast cells. Interestingly, three other known GATA motif-dependent Gata2 regulatory elements, the -1.8-, -2.8-, and -77-kb regions, which are important to regulate Gata2 in hematopoietic cells are not occupied by GATA factors in trophoblast cells. These elements do not show any enhancer activity and also possess inaccessible chromatin structure in trophoblast cells indicating a context-dependent function. Our results indicate that GATA3 directly represses Gata2 in undifferentiated trophoblast cells, and a switch in chromatin occupancy between GATA3 and GATA2 (GATA3/GATA2 switch) induces transcription during trophoblast differentiation. We predict that this GATA3/GATA2 switch is an important mechanism for the transcriptional regulation of other trophoblast-specific genes. 

Retracted: No

PubPeer comments:
 Figure 3B. Much more similar than expected. https: imgur.com YUdXl94 ,
Double‚Äênegative feedback interaction between DNA methyltransferase 3A and microRNA‚Ä?45 in the Warburg effect of ovarian cancer cells
Authors: Jie Li
Han Li
Meili Pei
Yanli Liu
Zhen Li
Songlin Zhang
Journal: Cancer Science (2018)
Discipline: CLINICAL MEDICINE
Keywords: DNMT3A; methylation; miR-145; ovarian cancer; the Warburg effect.
Affiliations: Department of Structural Heart Disease, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China., Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Abstract:  Ovarian cancer is the most lethal gynecological malignancy because of its poor prognosis. The Warburg effect is one of the key mechanisms mediating cancer progression. Molecules targeting the Warburg effect are therefore of significant therapeutic value for the treatment of cancers. Many microRNAs (miR) are dysregulated in cancers, and aberrant miR expression patterns have been suggested to correlate with the Warburg effect in cancer cells. In our study, we found that miR-145 negatively correlated with DNA methyltransferase (DNMT)3A expression at cellular/histological levels. miR-145 inhibited the Warburg effect by targeting HK2. Luciferase reporter assays confirmed that miR-145-mediated downregulation of DNMT3A occurred through direct targeting of its mRNA 3'-UTRs, whereas methylation-specific PCR (MSP) assays found that knockdown of DNMT3A increased mRNA level of miR-145 and decreased methylation levels of promoter regions in the miR-145 precursor gene, thus suggesting a crucial crosstalk between miR-145 and DNMT3A by a double-negative feedback loop. DNMT3A promoted the Warburg effect through miR-145. Coimmunoprecipitation assays confirmed no direct binding between DNMT3A and HK2. In conclusion, a feedback loop between miR-145 and DNMT3A is a potent signature for the Warburg effect in ovarian cancer, promising a potential target for improved anticancer treatment. 

Retracted: No

PubPeer comments:
 Figure 2 of this paper appears to overlap with an image from a different paper, [Li and Liu et al, 2014](http: www.spandidos-publications.com ijo 46 2 775)   Though the two papers have an author in common, the experiments are labeled as having used different treatments. , 
 #1 Thanks so much for pointing out these errors for us. After checking the data, we are so sorry not to notice the duplicated images. Because these experiments were done at the same time, there is a confusion of naming when saving picture, we will contact the editor as soon as possible to replace these images. Thanks again for your comments. We apologize for these mistakes to the journal editors, reviewers and readers for any inconvenience, and will pay attention to this and not make the same mistakes in the future. Best Wishes. ,
Anti-inflammatory and Antioxidant Properties of Probiotic Bacterium Lactobacillus mucosae AN1 and Lactobacillus fermentum SNR1 in Wistar Albino Rats
Authors: Venkatesan Arul
Repally Ayyanna
Dasari Ankaiah
Journal: Frontiers in Microbiology (2018)
Discipline: MICROBIOLOGY
Keywords: anti-inflammation; antioxidant activity; histopathology; immunohisto chemistry; interleukins
Affiliations: Department of Biotechnology, School of Life Sciences, Pondicherry University, Pondicherry, India.

Abstract:  The potent antioxidant probiotic strains Lactobacillus mucosae AN1 and Lactobacillus fermentum SNR1 were assessed for anti-inflammatory properties in carrageenan (acute) and complete Freund's adjuvant-induced inflammation (chronic) models in the present study. The two probiotic strains were administered orally along with feed to the Wistar albino male rats as whole cell as well as microencapsulated form. The following experiments were performed to evaluate the anti-inflammatory properties of probiotic strains and the results were observed that the encapsulated and unencapsulated probiotic strains have exhibited statistically significant decrease in paw thickness. Percentage of inhibition in paw thickness of microencapsulated probiotic bacteria (Group VIII), unencapsulated strains (Group IX) were revealed 85 ¬± 13% and 77 ¬± 25%, respectively. In Hematoxylin and Eosin staining, results were revealed that the probiotic strains were exhibited anti-inflammatory effects on inflammation-induced paw tissues. qRT-PCR studies revealed upregulation of anti-inflammatory cytokine genes and down-regulation pro-inflammatory cytokine genes in probiotic-treated rat paw tissues. Further, the expression of anti-inflammatory and pro-inflammatory cytokines were examined using immunohistochemistry and ELISA methods. The probiotic administered rat paw tissue in different groups have exhibited the low level of lipid peroxides formation and higher anti-oxidant activities when compared to the control and inflammation control tissues. 

Retracted: No

PubPeer comments:
 Figure 3. * In blue: Group IV; IL-10 appears to have an overlap with Group IV; IL-6. * In green: Group V; IL-10 appears to have an overlap with Group VII; IL-6. * In pink: Group IX; IL-10 appears to have an overlap with Group IX; IL-6.  ,
Suppression of Tafazzin promotes thyroid cancer apoptosis via activating the JNK signaling pathway and enhancing INF2‚Äêmediated mitochondrial fission
Authors: Xiaobin Li
Zengze Li
Ziwen Liu
Yimin Song
Mengwei Wu
Hongwei Yuan
Dawei An
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: INF2; JNK signaling pathway; Tafazzin; mitochondrial fission; thyroid cancer.
Affiliations: Department of General Surgery Peking Union Medical College Hospital, Chinese Academy of Medical Sciences &amp; Peking Union Medical College Beijing People‚Ä?Republic of China, Department of Public Relations Xinjiang Production and Construction Corps Hospital Urumqi People‚Ä?Republic of China

Abstract:  Tafazzin has been found to be associated with tumor progression. Mitochondrial homeostasis regulates cancer cell viability and metastasis. However, the roles of Tafazzin and mitochondrial homeostasis in thyroid cancer have not been explored. The aim of our study is to investigate the influences of Tafazzin on thyroid cancer apoptosis with a focus on mitochondrial fission. Our results indicated that Tafazzin deletion induced death in thyroid cancer via apoptosis. Biological analysis demonstrated that mitochondrial stress, including mitochondrial bioenergetics disorder, mitochondrial oxidative stress, and mitochondrial apoptosis, was activated by Tafazzin deletion. Furthermore, we found that Tafazzin affected mitochondrial stress by triggering inverted formin 2 (INF2)-related mitochondrial fission. The loss of INF2 sustained mitochondrial function and promoted cancer cell survival. Molecular investigation illustrated that Tafazzin regulated INF2 expression via the JNK signaling pathway; moreover, the blockade of JNK prevented Tafazzin-mediated INF2 expression and improved cancer cell survival. Taken together, our results highlight the key role of Tafazzin as a master regulator of thyroid cancer viability via the modulation of INF2-related mitochondrial fission and the JNK signaling pathway. These findings defined Tafazzin deletion and INF2-related mitochondrial fission as tumor suppressors that act by promoting cancer apoptosis via the JNK signaling pathway, with potential implications for new approaches to thyroid cancer therapy. 

Retracted: No

PubPeer comments:
 Figure 5H appears to have a splice. Could the authors please post the original uncropped scans? *** Inverse, contrast enhanced  *** Original  ,
Glucocorticoids regulate metallothionein-1/2 expression in rat choroid plexus: effects on apoptosis
Authors: I Gon√ßalves
C R Santos
A Martinho
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Choroid plexus; Metallothioneins; Glucocorticoids; Apoptosis; Central nervous system
Affiliations: CICS-UBI-Health Sciences Research Centre, University of Beira Interior, Covilh√£, Portugal.

Abstract:  The choroid plexus (CP) participates in the synthesis, secretion and regulation of the cerebrospinal fluid, in the removal of its toxic compounds and in the regulation of the availability of essential metal ions to the brain. It expresses and secretes metallothioneins 1/2 (MT-1/2) which are key components in the maintenance of the central nervous system metal homeostasis and have anti-apoptotic properties, thereby protecting the brain. Glucocorticoids regulate MT-1/2 expression in several brain regions, but within the choroid plexuses (CPs) it remains unknown. Glucocorticoid levels increase in response to stress with implications in apoptosis. Further, CP expresses glucocorticoid (GR) and mineralocorticoid receptors (MR) turning it into likely glucocorticoid responsive structure. Data prompted us to study the regulation of MT-1/2 expression in response to glucocorticoids in the rat CP, and to investigate its implications in apoptosis. MT-1/2 protein and mRNA expression analysis showed that hydrocortisone up-regulates MT-1/2 expression in rat choroid plexus (RCP) cell line and in primary cultures of choroid plexus epithelial cells (CPEC) cultures via GR and MR. Also, incubation of RCP cells with hydrocortisone significantly diminished apoptosis, an effect eliminated by the addition of a MT-1/2 antibody. Moreover, induction of psychosocial stress, with concomitant rise of corticosterone levels, increased MT-1/2 expression in liver and in CP of male and female rats, with an exception observed in CP from males subjected to acute stress in which down-regulation in MT-1/2 expression occurred. Altogether, the results obtained demonstrated that stress/glucocorticoids regulate MT-1/2 expression in rat CP, with implications on apoptosis. 

Retracted: No

PubPeer comments:
 Figure 2A. * Red boxes: The 12h and 36h b-actin panels appear to look more similar than expected. Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. I would love to hear from the authors if the journal ever contacted them in the past five years.  ,
Sodium Channel Subunit SCNN1B Suppresses Gastric Cancer Growth and Metastasis via GRP78 Degradation
Authors: Hua Wang
Li Zhang
Minnie Y Y Go
Philip W Y Chiu
Wei Kang
Joseph J Y Sung
Jun Yu
Weilin Li
Huarong Chen
Enders K W Ng
Jiaying Xu
Yun Qian
Jianmin Si
Yanquan Zhang
Francis K L Chan
Eagle S H Chu
Chi Chun Wong
Journal: Cancer Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: functional biomarkers; gastric cancer; SCNN1B; mRNA expression; promoter hypermethylation
Affiliations: Institute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China., School of Biomedical Science, The Chinese University of Hong Kong, Hong Kong, China., Department of Surgery, The Chinese University of Hong Kong, Hong Kong, China., Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China., Institute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China. .

Abstract:  There remains a paucity of functional biomarkers in gastric cancer. Here, we report the identification of the sodium channel subunit SCNN1B as a candidate biomarker in gastric cancer. SCNN1B mRNA expression was silenced commonly by promoter hypermethylation in gastric cancer cell lines and primary tumor tissues. Tissue microarray analysis revealed that high expression of SCNN1B was an independent prognostic factor for longer survival in gastric cancer patients, especially those with late-stage disease. Functional studies demonstrated that SCNN1B overexpression was sufficient to suppress multiple features of cancer cell pathophysiology in vitro and in vivo Mechanistic investigations revealed that SCNN1B interacted with the endoplasmic reticulum chaperone, GRP78, and induced its degradation via polyubiquitination, triggering the unfolded protein response (UPR) via activation of PERK, ATF4, XBP1s, and C/EBP homologous protein and leading in turn to caspase-dependent apoptosis. Accordingly, SCNN1B sensitized gastric cancer cells to the UPR-inducing drug tunicamycin. GRP78 overexpression abolished the inhibitory effect of SCNN1B on cell growth and migration, whereas GRP78 silencing aggravated growth inhibition by SCNN1B. In summary, our results identify SCNN1B as a tumor-suppressive function that triggers UPR in gastric cancer cells, with implications for its potential clinical applications as a survival biomarker in gastric cancer patients. Cancer Res; 77(8); 1968-82. ¬©2017 AACR. 

Retracted: No

PubPeer comments:
 In Figure 3A, some photo images were duplicated.  ,
Stress-induced anhedonia is associated with an increase in Alzheimer's disease-related markers
Authors: R Tordera
E Martisova
M Dobarro
S Gagno
B Aisa
Mj Ram√≠rez
M Solas
A Briones
Journal: British Journal of Pharmacology (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Stress; Neuropsychiatric disorders; Alzheimer's disease; Chronic mild stress; Vulnerability

Abstract:  Background and purpose: Stress is believed to be associated with the development of neuropsychiatric disorders, including Alzheimer's disease (AD). We have studied mechanisms implicated in vulnerability to stress and the relationship with changes in AD-related markers. Experimental approach: Anhedonia induced by a chronic mild stress (CMS) procedure, applied for 6 weeks, was used to select rats vulnerable or resistant to stress. Sucrose intake, the Porsolt forced swimming test and cognitive deficits in the novel object recognition test (NORT) were used to characterize vulnerable and resilient rats. The antidepressant venlafaxine (20 mg¬∑kg(-1) p.o.) or saline was administered daily during the last 2 weeks of CMS. Biochemical markers affected by stress, PKB, ERK and synaptophysin, and those associated with AD, amyloid Œ≤-protein (AŒ≤), Œ≤-secretase (BACE1) and œÑ phosphorylation, were measured in the hippocampus. Key results: After CMS, 40% of rats were resistant to the development of anhedonia (CMS-resistant to stress), whereas the remaining were responsive [CMS-anhedonic (CMSA)]. Only CMSA rats displayed significant increases in immobility time in the forced swimming test and cognitive deficits in the NORT, and significant decreases in synaptophysin, phosphorylated PKB and phosphorylated ERK1/2 expression in the hippocampus. Increased levels of AŒ≤40, BACE1 and œÑ phosphorylation were also found only in CMSA rats. All these effects in CMSA rats were reverted by treatment with venlafaxine. Conclusions and implications: Vulnerability to stress might constitute a risk factor for the development of AD, and pharmacological treatment with venlafaxine may represent a therapeutic strategy for the treatment of stress-related disorders, including AD. 

Retracted: No

PubPeer comments:
 There appears to be multiple duplications in the western blots in Figure 6.   Could the authors perhaps look into this? Were the wrong blots uploaded, or is it perhaps a trick of the compression algorithm. Do they still have high resolution scans of the original blots? ,
Zn(II)-Based Coordination Polymer for Detection of Picric Acid in Aqueous Media and Treatment Effect against Deep Vein Thrombosis by Reducing P-ERK2 and p53 Expression
Authors: Yinhua Cheng
Peng Li
Weiwei Song
Shasha Song
Journal: Journal of Fluorescence (2020)
Discipline: CHEMISTRY
Keywords: Deep vein thrombosis; N-donor sites; Porous structure; TNP detection; Zn(II)-framework.
Affiliations: Emergency Department, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China., Department of Surgery, Laishan Branch of Yuhuangding Hospital, Yantai, Shandong, China., Spinal Surgery Department, Jinan Fourth People's Hospital, Jinan, Shandong, China., Spinal Surgery Department, Jinan Fourth People's Hospital, Jinan, Shandong, China. .

Abstract:  The coordination polymers based on Zn(II) ions and the metal nodes which has chemical formula of {[Zn3(L)2(tib)2(H2O)2]¬∑(DMF)2}n (1) was synthesized via using 1,3,5-tris(1-imidazolyl)benzene (tib) and 2,6-di(4-carboxylphenyl)pyridine-4-carboxylic acid (H3L) as ligands under solvothermal conditions. Given its strong luminescent emission at room temperature and the uncoordinated N-donor sites in the framework, the selective detection performance of 1 toward the nitroanalytes was studied, 1's sensitive fluorescence quenching reactions along with selectivity to the electron-deficient TNP over other analytes of nitro within the aqueous phase was studied via the method of fluorescence quenching titration. Furthermore, the treatment effect of the compound on the deep vein thrombosis (DVT) was evaluated. Firstly, the ELISA was carried out to determine IL-17A content. Then, the platelet function was determined via the western blot by measuring expression level of platelet activation signaling pathway protein p-ERK2 and p53. 

Retracted: No

PubPeer comments:
  Detection of Picric Acid in Aqueous Media and Treatment Effect against Deep Vein Thrombosis  It s a floor-polish AND a dessert topping! ----------------------------------------------  There is no specific body area limitation within the deep vein thrombosis development, and bodyu2019s main vein can produce the disease under certain conditions [4]. - [4]. Liu W, Li H, Zhu H, Xu P (2020) **The interfacial adhesion performance and mechanism of a modified asphaltu2013steel slag aggregate**. Materials 13:1180  The most common manifestations are femoral vein thrombosis, inferior vena cava thrombosis as well as lower extremity venous thrombosis, all of which could cause serious harm to patients [5]. - [5]. Wang Z, Zhang X, Jiang S, Qu Y, Ou D, Wang J (2020) **Arc erosion dynamic of island-and skeleton-restricted microstructure evolution modes in Agu2013CuO contact materials**. J Alloy Compd 828:154412 I have nothing to add. , 
  A mouse DVT model was constructed by narrowing the inferior vena cava . Just like that. No more details. ,
MiRNA-545 negatively regulates the oncogenic activity of EMS1 in gastric cancer
Authors: Chaohui Zuo
Ke Xiao
Min Ma
Juanxia Zhao
Qunfeng Wu
Shuang Li
Chen Liu
Haizhen Zhu
Hailong Xie
Journal: Cancer Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: Cell proliferation; EMS1; EMT process; gastric cancer; miR-545.
Affiliations: The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Hunan Cancer Hospital, Changsha, Hunan, 410013, China., Institute of Cancer Research, School of Medicine, University of South China, Hengyang, Hunan, 421001, China., Department of Pathology and Laboratory Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, New Jersey, 07103., Department of Molecular Medicine, College of Biology, State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha, Hunan, 410082, China.

Abstract:  Gastric cancer (GC) is a common malignant tumor of the digestive system. In addition, GC metastasis is an extremely complicated process. In this article, high expression levels of EMS1 mRNA and protein were found to be positively correlated with an enhanced malignant potential of GC cells and a poor clinical prognosis of GC patients. Interestingly, the expression levels of EMS1 mRNA and protein in GC cells were inhibited by microRNA-545 (miR-545), which was identified by a bioinformatics analysis. The expression level of miR-545 in carcinoma tissues was significantly lower than that in para-carcinoma tissues. The proliferation and epithelial-mesenchymal transition (EMT) of GC cells were suppressed by exogenous oligonucleotides of miR-545 mimics. In addition, the expression levels of EMT-associated markers were altered with the expression of miR-545. Notably, the growth rates of tumors in nude mice were seriously restrained by an intratumoral injection of oligonucleotides of the miR-545 mimics. These results suggest a negative regulatory role of miR-545 on the oncogenic activity of EMS1. In addition, EMS1 and miR-545 may be potential biomarkers for GC diagnosis. Synthesized oligonucleotides of miR-545 mimics may be developed as important gene medicines for GC therapy in the future. 

Retracted: No

PubPeer comments:
 Figure 3A and 3B appear to have some duplicated images. In the case of the images marked with purple boxes, the measurement lines appear to be different. ***  , 
 Two images in Figure 3C and 3D appear to overlap. ***  , 
 In the interest of thoroughness, it appears that some images in this paper also appear in a paper that was published later. That paper is discussed in another thread: https: pubpeer.com publications 9F5D26FDF83E716B615F407B35ED8B ***  ,
Divergent roles of amino acid residues inside and outside the BB loop affect human Toll-like receptor (TLR)2/2, TLR2/1 and TLR2/6 responsiveness
Authors: Yuan Qiu
Wenyue Xu
Zhangping Tan
Yan Ding
Taiping Liu
Lingyun Zou
Xiaolan Fu
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: TLR2; ligands; signalling transduction; amino acid residues; TLR1
Affiliations: Department of Pathogenic Biology, Third Military Medical University, Chongqing, P. R. China.

Abstract:  TLR2 specifically recognizes a wide range of ligands by homodimerizing or heterodimerizing with TLR1 or TLR6. However, the molecular basis of the specific signalling transduction induced by TLR2 homodimerization or heterodimerization with TLR1 or TLR6 is largely unknown. In this study, we found three amino acid residues, two (663L and 688N) outside and one (681P) inside the BB loop, which were conserved in all of the TLRs, except for the TLR3 toll/IL-1R(TIR) domain. The responsiveness of human TLR2/2, TLR2/1 or TLR2/6 was completely lost when 663L and 688N were replaced with the corresponding amino acid residues in the TLR3 TIR domain, respectively. However, the response of TLR2 (P681A) to the high concentration of TLR2/TLR6 agonist was almost intact, but the activity of TLR2 (P681A) was greatly reduced when stimulated with the TLR2/1 agonist or the TLR2/2 agonist. Although the surface expression of TLR2 (L663E) was sharply reduced, both the intracellular distribution and the surface expression of all of the other TLR2 mutants were unchanged. The ability of all three TLR2 mutants to recruit MyD88, was consistent with their responsivenesses. Computer modelling indicated that the surface negative charge of all of the TLR2 mutants' BB loops was reduced. Thus, our data demonstrated that the 663L and 688N residues outside of the BB loop were essential for the responsiveness of TLR2/2, TLR2/1 and TLR2/6, but the 681P residue inside of the BB loop exhibited divergent roles in TLR2/2, TLR2/1 and TLR2/6 signalling transduction, thereby providing clues regarding the specific signalling transduction of TLR2/2, TLR2/1 and TLR2/6. 

Retracted: No

PubPeer comments:
 Figure 4D. * Red arrows: Lanes 1-2 in the actin panel look similar to lanes 4 and 5. A sharp vertical background transition is noted between lanes 3 and 4.  This concern was reported to the journal in 2015, with a friendly reminder in 2016, but no response so far. ,
Natural killer cell-derived exosome-entrapped paclitaxel can enhance its anti-tumor effect
Authors: K Wang
T Zhang
H Xu
G-C Gao
D Han
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Natural killer cell-derived exosome; paclitaxel; anti-tumor effect; drug delivery system; MCF-7 cells
Affiliations: Jiaxing University, Jiaxing, Zhejiang, China. .

Abstract:  Objective: To study the effectiveness of natural killer cell-derived exosome (NK-Exos)-entrapped paclitaxel (PTX-NK-Exos) in enhancing its anti-tumor effect. Materials and methods: The NK-Exos were isolated through ultra-high-speed centrifugation, and the PTX-NK-Exos system was constructed via electroporation. The morphology, particle size, Zeta potential and entrapment rate of PTX-NK-Exos were evaluated using transmission electron microscope (TEM), dynamic light scattering (DLS), Western blotting and high-performance liquid chromatography (HPLC), respectively. The uptake of Exos in human breast cancer MCF-7 cells was observed under a laser confocal microscope. Moreover, the effect of PTX-NK-Exos on MCF-7 cell viability was determined through methyl thiazolyl tetrazolium (MTT) assay, flow cytometry and 4',6-diamidino-2-phenylindole (DAPI) staining. The effects of PTX-NK-Exos on messenger ribonucleic acid (mRNA) and protein expressions of B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax) and Caspase-3 in MCF-7 cells were detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting, respectively. Results: The NK-Exos were successfully isolated via ultra-high-speed centrifugation, and they had uniform particle size and high expression of markers for Exos. MCF-7 cells could take up Exos. The PTX-NK-Exos drug delivery system was successfully prepared using electroporation. In PTX group and NK-Exos group, the proliferation of MCF-7 cells declined, the nuclear apoptosis was evident and the apoptosis rate of MCF-7 cells rose compared with those in Control group. In PTX group and PTX-NK-Exos group, the migration of MCF-7 cells declined compared with that in Control group. According to the results of qRT-PCR and Western blotting, PTX-NK-Exos exerted an anti-tumor effect through inducing the up-regulation of Bax and Caspase-3 in the apoptotic signaling pathway in tumor cells. Conclusions: Exos isolated through ultra-high-speed centrifugation can be used to prepare the PTX-NK-Exos drug delivery system through electroporation. Drug-loaded Exos can effectively inhibit proliferation and induce apoptosis of tumor cells, thereby exerting an anti-tumor effect. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: In the top row (0h) the left (NK-Exos) and middle (PTX) panel look very similar.  ,