PReD-Bench/PRed-Bench huggingface dataset:
Long circulating chitosan/PEG blended PLGA nanoparticle for tumor drug delivery
Authors: Suphiya Parveen
Sanjeeb K Sahoo
Journal: European Journal of Pharmacology (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Polymeric nanoparticles; drug delivery; chitosan; polyethylene glycol; PLGA
Affiliations: Laboratory of Nanomedicine, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar, India.

Abstract:  Polymeric nanoparticles have long been sought after as carriers for systemic and targeted drug delivery. The ability of these particles to circulate in the bloodstream for a prolonged period of time is often a prerequisite for successful targeted delivery. To achieve this, paclitaxel loaded chitosan and polyethylene glycol coated PLGA (PLGA-CS-PEG) nanoparticles were formulated and characterized that could efficiently encapsulate hydrophobic drugs, and also evade the phagocytic uptake by reducing opsonization by blood proteins, hence increasing the bioavailability of the drug. In our study, we primarily assessed a rational approach for designing and formulating ideal long-circulating nanoparticles by optimizing the concentration of chitosan (CS) and polyethylene glycol (PEG). Uptake efficiency and in vitro cytotoxicity of the formulated nanoparticles was also evaluated in different cancer cell lines (retinoblastoma, breast cancer and pancreatic cancer). PLGA-CS-PEG nanoparticles showed dramatic prolongation in blood circulation, as well as reduced macrophage uptake, with only a small amount of the nanoparticles sequestered in the liver, when compared to PLGA-CS and PLGA nanoparticles. Superior anti-proliferative effect and cell cycle inhibition was observed in case of PLGA-CS nanoparticles and PLGA-CS-PEG nanoparticles over PLGA nanoparticles and native paclitaxel, which may be due to higher cellular uptake resulting in greater antiproliferative activity of nanoparticles. The present results thus suggest that, a combinational coating of PEG and chitosan may represent a significant step in the development of long-circulating drug delivery carriers for tumor drug delivery. 

Retracted: No

PubPeer comments:
 Corrected [March 2014] . Old news, but not previously flagged at PubPeer. --------------------------------------------- In Fig. 2(A) the TEM image of PLGA nanoparticles should be as follows. ![file] Fig. 2. (A) PLGA nanoparticles. The error does not affect the conclusions drawn from this study. The authors would like to apologize for any inconvenience caused. --------------------------------------------------------------- The paper was the subject of [an anonymous blogpost](http: sk-sahoo.blogspot.com 2013 05 eur-j-pharmacol-2011-nov-306702-3372-83.html), focusing on the previous appearance of Fig 2A in an earlier publication ([Misra Sahoo 2010] ) with a different identification. ![file] ,
Ectopic PDX-1 expression in liver ameliorates type 1 diabetes
Authors: Shira Perl
Irun R Cohen
Iris Barshack
Francisco J Quintana
Sarah Ferber
Irit Meivar-Levy
Keren Shternhall-Ron
Journal: Journal of Autoimmunity (2007)
Discipline: IMMUNOLOGY
Keywords: Type 1 diabetes mellitus; autoimmune; pancreatic beta-cells; PDX-1; liver cells
Affiliations: The Endocrine Institute, Sheba Medical Ctr., Tel-Hashomer 52621, Israel.

Abstract:  Type 1 diabetes mellitus (T1DM) results from a specific autoimmune mediated destruction of the pancreatic beta-cells. PDX-1 induced developmentally redirected liver cells were suggested to restore the ablated pancreatic function in chemically induced diabetes. However, developmentally redirected liver cells, may have acquired along with the desired beta-cell characteristics and functions, also undesired sensitivity to autoimmune attack and therefore may be inefficient in ameliorating T1DM. This study analyzes whether subjects with beta-cell autoimmunity could benefit from Ad-CMV-PDX-1 gene therapy. Using the model of cyclophosphamide-accelerated diabetes in non-obese diabetic (CAD-NOD) mice, we report that recombinant adenovirus mediated PDX-1 gene therapy, ameliorates hyperglycemia in CAD-NOD mice. Our data demonstrate that 43% of the overtly diabetic CAD-NOD mice treated with Ad-CMV-PDX-1 became normoglycemic and maintained a stable body weight. Ectopic PDX-1 expression induced pancreatic gene expression and insulin production in the mice livers. The amelioration of hyperglycemia, in PDX-1 treated diabetic mice was associated with an immune modulation manifested by Th1 to Th2 shift in the autoimmune T-cell response to antigens associated with NOD diabetes. Thus, liver-to-pancreas transdifferentiation ameliorates T1DM in a process which is associated with a concomitant modulation of the autoimmune attack. Our findings suggest a beneficial therapeutic effect of the PDX-1 gene therapy for treating autoimmune type 1 diabetes mellitus (T1DM). 

Retracted: No

PubPeer comments:
 In Fig. 1a of this paper, the RT-PCR gel slices share many of the same bands. After levels adjustment, pasting edges can also be viewed. ![image] , 
 Does the Journal of Autoimmunity publish novel research or does it simply rehash what has already been published elsewhere? Not only does Fig. 1A have all those in-figure band duplications shown above, it also borrows some bands from a paper published 4 years earlier in JBC. In a paper with manifest problems of its own https: pubpeer.com publications 2F98A5FD4DA9573BF72B695788CC73 To keep things simple while getting started, here is a PDX-1 band reuse ![image] , 
 The co-Editor-in-Chief could mosey on down the corridor and check out the image issues himself. Whereas six bands are being compared in these RT-PCR duplications, only four of them are the same as before. It is a mystery as to why glucagon and somatostatin needed to have different bands pasted into their gels when the others didnu2019t. ![image] , 
 Looking at the control lanes, three gel slices show reuse and three do not. ![image] ,
99mTc-DTPA-amino acids conjugate as specific SPECT pharmaceuticals for tumor imaging
Authors: Shubhra Chaturvedi
Anil K Mishra
Krishna Chuttani
Gauri Shukla
Anjani K Tiwari
Harish Chandra
Deepa Sinha
Journal: Chemical Biology & Drug Design (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: (99m)Tc-Diethylene triamine pentaacetic acid-bis (amide) conjugates; radiopharmaceutical; tumor imaging; synthesis; characterization
Affiliations: Division of Cyclotron and Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, Delhi, India.

Abstract:  (99m)Tc-Diethylene triamine pentaacetic acid-bis (amide) conjugates have been synthesized and evaluated as a potential radiopharmaceutical for tumor imaging. The compounds were synthesized by the condensation reaction of DTPA bis(anhydride) with different l-amino acids (methyl tryptophan, and 5-hydroxy tryptophan) and were characterized on the basis of IR, NMR, and Mass spectroscopy. (99m)Tc-labeled compounds were found stable for about 24 h under physiological conditions with more than 95% radiolabeling yield. Blood kinetic studies of all these complexes showed a bi-exponential pattern as well as quick wash out from the blood circulation. The biological t(1/2)(F) and t(1/2)(S) were found to be 20 +/- 0.001 min for DTPA-(Me-Trp)(2) and 18 +/- 0.001 min for DTPA-(5HT)(2) and t(1/2) (slow) 5 h 45 min +/- 0.001, 5 h 30 +/- 0.001 min for DTPA-(Me-Trp)(2), and DTPA-(5HT)(2), respectively. Imaging and biodistribution studies were performed in mice bearing Ehrlich ascites tumor (EAT) tumors in right thigh. Radioconjugate derived from l-5-hydroxytryptophan exhibited remarkable localization at tumor site; whereas radiotracer derived from l-methyl tryptophan shows relatively less accumulation at the tumor site. Tumor-to-muscles ratios were 5.07 +/- 0.001, and 4.2 +/- 0.001 at 1 and 4 h for (99m)Tc-DTPA-(Me trp)(2) and 4.97 +/- 0.001 and 5.8 +/- 0.001 at 1 and 4 h after postinjection for (99m)Tc-DTPA-(5HT)(2), respectively. The preliminary results with these amino acid based ligands are encouraging to carrying out further in vivo experiments for targeted tumor imaging. 

Retracted: No

PubPeer comments:
 A strange uniformity in the SD values of 11 organs and that is up to the third decimal level? ![file] ,
miR‑365 overexpression promotes cell proliferation and invasion by targeting ADAMTS-1 in breast cancer
Authors: Lulu Liu
Wenqiao Zang
Guoqiang Zhao
Yuwen Du
Xiaonan Chen
Ping Li
Juan Li
Min Li
Yuanyuan Wang
Journal: International Journal of Oncology (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-365; breast cancer; cell growth; cell cycle
Affiliations: College of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, P.R. China., Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China.

Abstract:  MicroRNAs (miRNAs) have important roles in the initiation and progression of human cancer, including breast cancer. We evaluated miR‑365 expression in breast cancer tissues, and investigated its effects on cell growth, cell cycle, cell invasion, and expression of its target gene ADAMTS-1. miR‑365 expression levels were analyzed in breast cancer tissues and adjacent normal tissues using qRT-PCR. CCK-8, cell cycle, and invasion assays were used to explore the role of miR‑365 expression in breast cancer cells. We conducted luciferase reporter and western blot assays to test whether ADAMTS-1 is a direct target of miR‑365. We found that miR‑365 expression levels were significantly higher in breast cancer tissues compared with adjacent non-tumor tissues (P&lt;0.05). These relatively high expression levels were significantly associated with advanced clinical stages (P&lt;0.05). In breast cancer cell lines, transfection with miR‑365 inhibitor suppressed proliferation and invasion, and resulted in cell cycle arrest. Subsequent experiments indicated that miR‑365 bound the 3'-UTR of ADAMTS-1 and downregulated its expression. Our findings indicated that the inhibition of miR‑365 reduced cell proliferation and cell invasion. Additionally, miR‑365 may function as a novel oncogene in breast cancer through targeting ADAMTS-1. These findings provide insight into the mechanism of breast cancer pathogenesis. 

Retracted: No

PubPeer comments:
  Figure 3. Effect of miR-365 downregulation on cell cycle progression in MDA-MB-231 and MCF-7 cells. (A) Cell cycle distribution was analyzed by flow cytometry Results for NC and Blank controls for MCF-7 appear to be the same, except for the marked area. ![file] , 
 [Perhaps a systemic problem] . Journals and readers may wish to proceed with caution. ,
Binding Studies of TNF Receptor Superfamily (TNFRSF) Receptors on Intact Cells
Authors: Andrea Fick
Agnes Wyzgol
Johannes Trebing
Daniela Weisenberger
José Antonio Carmona Arana
Harald Wajant
Simone Füllsack
Viktoria Schäfer
Isabell Lang
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: NF-κB (NF-KB); TNF receptor-associated factor; cytokine; fusion protein; ligand-binding protein
Affiliations: From the Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Würzburg, Röntgenring 11, 97070 Würzburg, Germany., From the Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Würzburg, Röntgenring 11, 97070 Würzburg, Germany .

Abstract:  Ligands of the tumor necrosis factor superfamily (TNFSF) interact with members of the TNF receptor superfamily (TNFRSF). TNFSF ligand-TNFRSF receptor interactions have been intensively evaluated by many groups. The affinities of TNFSF ligand-TNFRSF receptor interactions are highly dependent on the oligomerization state of the receptor, and cellular factors (e.g. actin cytoskeleton and lipid rafts) influence the assembly of ligand-receptor complexes, too. Binding studies on TNFSF ligand-TNFRSF receptor interactions were typically performed using cell-free assays with recombinant fusion proteins that contain varying numbers of TNFRSF ectodomains. It is therefore not surprising that affinities determined for an individual TNFSF ligand-TNFRSF interaction differ sometimes by several orders of magnitude and often do not reflect the ligand activity observed in cellular assays. To overcome the intrinsic limitations of cell-free binding studies and usage of recombinant receptor domains, we performed comprehensive binding studies with Gaussia princeps luciferase TNFSF ligand fusion proteins for cell-bound TNFRSF members on intact cells at 37 °C. The affinities of the TNFSF ligand G. princeps luciferase-fusion proteins ranged between 0.01 and 19 nm and offer the currently most comprehensive and best suited panel of affinities for in silico studies of ligand-receptor systems of the TNF family. 

Retracted: No

PubPeer comments:
 The immunoblot for p100 and p52 of different groups in red boxes in Fig 3 appear to look similar. ![file] , 
 #1 Thank you for pointing out. The two WBs do indeed look similar. We will seek out and review the original laboratory documents to clarify this and, if necessary, to contact JBC. Best regards HW , 
 Dear Proctacanthus Coquilletti, We checked the original blots and you are right, the Flag-TNC-CD40L WB was mistakenly used again for the Flag-TNC-CD27L WB. We contact JBC with the request for a corresponding correction. With kind regards HW , 
 JBC has approved to publish a correction note. Kind regards HW , 
 2020 correction. https: www.jbc.org content 295 32 11377.short During preparation of Fig. 3, the p100 p52 immunoblot of Flag-TNC-CD27Lu2013treated cells was inadvertently used in the Flag-TNC-CD40L immunoblot panel. This error has now been corrected and does not affect the results or conclusions of this work. The authors apologize for the error. ,
Glycoprotein-based enzyme-linked immunosorbent assays for serodiagnosis of infectious laryngotracheitis
Authors: Mallikarjuna Kanabagatte Basavarajappa
Chinta Lamichhane
Siba K Samal
Haichen Song
Journal: Journal of clinical microbiology (2015)
Discipline: MICROBIOLOGY
Keywords: ILTV; antibody detection; ELISA; glycoprotein B; glycoprotein C
Affiliations: Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, Maryland, USA., Zoetis, College Park, Maryland, USA., Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, Maryland, USA .

Abstract:  For detection of infectious laryngotracheitis virus (ILTV) antibody, glycoprotein B-, C-, and D-based enzyme-linked immunosorbent assays (B-, C-, and D-ELISAs, respectively) were developed. The B- and D-ELISAs showed enhanced detection of anti-ILTV antibodies in infected chickens compared to that of the commercial ELISA. Furthermore, the D-ELISA was efficient in detecting seroconversion with vectored vaccine, using recombinant Newcastle disease virus (rNDV) expressing glycoprotein D (gD) as the vaccine vector. 

Retracted: Yes

PubPeer comments:
null, 
 2020 retraction. https: jcm.asm.org content 58 3 e01820-19 Page 1729, Fig. 2A: It has been called to our attention that lanes 1 and 2 are duplicated. Unfortunately, the laboratory no longer has the samples to validate the published figure. Since we cannot perform the experiment, we retract this paper. ,
Osmotherapy With Hypertonic Saline Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest via Perivascular Pool of Aquaporin-4
Authors: Ole P Ottersen
Shin Nakayama
Anish Bhardwaj
Elton Migliati
Mahmood Amiry-Moghaddam
Journal: Critical care medicine (2016)
Discipline: CLINICAL MEDICINE
Keywords: osmotherapy; hypertonic saline; cerebral edema; aquaporin-4; cardiac arrest
Affiliations: 1Departments of Neurology, Neurological Surgery and Anesthesiology and Peri-Operative Medicine, Oregon Health and Science University, Portland, OR. 2Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Abstract:  Objectives: We tested the hypothesis that osmotherapy with hypertonic saline attenuates cerebral edema following experimental cardiac arrest and cardiopulmonary resuscitation by exerting its effect via the perivascular pool of aquaporin-4. We used mice with targeted disruption of the gene encoding α-syntrophin (α-Syn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot and ependymal pools. Design: Laboratory animal study. Setting: University animal research laboratory. Interventions: Isoflurane-anesthetized adult male wild-type C57B/6 or α-Syn mice were subjected to cardiac arrest/cardiopulmonary resuscitation and treated with either a continuous IV infusion of 0.9% saline or various concentrations of hypertonic saline. Serum osmolality, regional brain water content, blood-brain barrier disruption, and aquaporin-4 protein expression were determined at 24 hours after cardiac arrest/cardiopulmonary resuscitation. Measurements and main results: Hypertonic saline (7.5%) treatment significantly attenuated water content in the caudoputamen complex and cortex compared with 0.9% saline treatment in wild-type mice subjected to cardiac arrest/cardiopulmonary resuscitation. In contrast, in α-Syn mice subjected to cardiac arrest/cardiopulmonary resuscitation, 7.5% hypertonic saline treatment did not attenuate water content. Treatment with 7.5% hypertonic saline attenuated blood-brain barrier disruption at 24 hours following cardiac arrest/cardiopulmonary resuscitation in wild-type mice but not in α-Syn mice. Total aquaporin-4 protein expression was not different between 0.9% saline and hypertonic saline-treated wild-type mice. Conclusions: Following experimental cardiac arrest/cardiopulmonary resuscitation: 1) continuous hypertonic saline therapy maintained to achieve serum osmolality of ≈ 350 mOsm/L is beneficial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role in water egress from brain; and 3) hypertonic saline attenuates blood-brain barrier disruption via perivascular aquaporin-4 pool. 

Retracted: No

PubPeer comments:
 Blots has been extensively cut and paste (red boxes) - original blots to be shown. Quantififaction (blue box) - how can this generate a higher value than the data to the right? The Standard deviation is low. What is the scale on the y-axes? What is p=0223? ![file] ,
Minimum Determinants of Transmissible Gastroenteritis Virus Enteric Tropism Are Located in the N-Terminus of Spike Protein
Authors: Sonia Zuñiga
Carlos M Sanchez
Isabel Sola
Alejandro Pascual-Iglesias
Luis Enjuanes
Journal: Pathogens (2019)
Discipline: MICROBIOLOGY
Keywords: enteric tropism; recombinant virus; transmissible gastroenteritis virus; tropism.
Affiliations: Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Campus Universidad Autónoma de Madrid, Darwin 3, 28049 Madrid, Spain.

Abstract:  Transmissible gastroenteritis virus (TGEV) is an enteric coronavirus causing high morbidity and mortality in porcine herds worldwide, that possesses both enteric and respiratory tropism. The ability to replicate in the enteric tract directly correlates with virulence, as TGEVs with an exclusive respiratory tropism are attenuated. The tissue tropism is determined by spike (S) protein, although the molecular bases for enteric tropism remain to be fully characterized. Both pAPN and sialic acid binding domains (aa 506-655 and 145-155, respectively) are necessary but not sufficient for enteric tract infection. Using a TGEV infectious cDNA and enteric (TGEV-SC11) or respiratory (TGEV-SPTV) isolates, encoding a full-length S protein, a set of chimeric recombinant viruses, with a sequential modification in S protein amino terminus, was engineered. In vivo tropism, either enteric, respiratory or both, was studied by inoculating three-day-old piglets and analyzing viral titers in lung and gut. The data indicated that U655&gt;G change in S gene (S219A in S protein) was required to confer enteric tropism to a respiratory virus that already contains the pAPN and sialic acid binding domains in its S protein. Moreover, an engineered virus containing U655&gt;G and a 6 nt insertion at position 1124 (Y374-T375insND in S protein) was genetically stable after passage in cell cultures, and increased virus titers in gut by 1000-fold. We postulated that the effect of these residues in enteric tropism may be mediated by the modification of both glycosaminoglycan binding and S protein structure. 

Retracted: No

PubPeer comments:
 Here s a [pre-print of 30 nCoV] genomes from GISAID - showing large changes in the Nterminal of the spike protein (corroborating this study) This is a [500bp fragment] unique to the 2019-nCov ,
Regulation of the adaptation to ER stress by KLF4 facilitates melanoma cell metastasis via upregulating NUCB2 expression
Authors: Dongmei Zhang
Jingrong Lin
Lu Zhang
Yulin Chao
Lei Jin
Na Li
Ruiping He
Chuanchun Han
Binbin Ma
Wenzhi Zhao
Journal: Journal of Experimental & Clinical Cancer Research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Apoptosis; ER stress; KLF4; Melanoma; Metastasis.
Affiliations: Institute of Cancer Stem Cell, Dalian Medical University, Dalian, 116044, China., Department of Physiology, College of Basic Medical Sciences, Dalian Medical University, Dalian, 116044, China., Department of Dermatology, the First Affiliated Hospital, Dalian Medical University, Liaoning, 116027, China., Department of Orthopedics, Second Affiliated Hospital, Dalian Medical University, Dalian, 116044, China., Department of Orthopedics, Second Affiliated Hospital, Dalian Medical University, Dalian, 116044, China. ., Institute of Cancer Stem Cell, Dalian Medical University, Dalian, 116044, China. .

Abstract:  Background: Adaptation to ER stress has been indicated to play an important role in resistance to therapy in human melanoma. However, the relationship between adaptation to ER stress and cell metastasis in human melanoma remains unclear. Methods: The relationship of adaptation to ER stress and cell metastasis was investigated using transwell and mouse metastasis assays. The potential molecular mechanism of KLF4 in regulating the adaptation to ER stress and cell metastasis was investigated using RNA sequencing analysis, q-RT-PCR and western blot assays. The transcriptional regulation of nucleobindin 2 (NUCB2) by KLF4 was identified using bioinformatic analysis, luciferase assay, and chromatin immunoprecipitation (ChIP). The clinical significance of KLF4 and NUCB2 was based on human tissue microarray (TMA) analysis. Results: Here, we demonstrated that KLF4 was induced by ER stress in melanoma cells, and increased KLF4 inhibited cell apoptosis and promoted cell metastasis. Further mechanistic studies revealed that KLF4 directly bound to the promoter of NUCB2, facilitating its transcription. Additionally, an increase in KLF4 promoted melanoma ER stress resistance, tumour growth and cell metastasis by regulating NCUB2 expression in vitro and in vivo. Elevated KLF4 was found in human melanoma tissues, which was associated with NUCB2 expression. Conclusion: Our data revealed that the promotion of ER stress resistance via the KLF4-NUCB2 axis is essential for melanoma cell metastasis, and KLF4 may be a promising specific target for melanoma therapy. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have two sets of image overlaps (with one slightly resized). *** ![file] ![file] , 
 #1 #1 I am sorry for it , we finished the assay using Me1007 in the figure 1A and 1C together. Therefore, we chose the image which has overlaps. In the figure 1a, I made mistakes for mel-cv and sk-mel-28 cells. I will correct it. , 
 #2 Thank you for responding. From the description I believed that Me1007 in 1c was treated with TM. ,
An efficient post-processing adaptive filtering technique to rectifying the flickering effects
Authors: Yunyoung Nam
Mohamed Abouhawwash
Jagroop Singh Sidhu
Sahil Verma
N Z Jhanjhi
Anudeep Gandam
Anand Nayyar
Journal: PLoS ONE (2021)
Discipline: Multidisciplinary
Keywords: Compression; Video frames; Pre-and post-processing technique; Quantization error; Ringing
Affiliations: Department of Electronics and Communication Engineering, IKG-Punjab Technical University Jalandhar, Punjab, India., Department of Electronics and Communication Engineering, DAVIET Jalandhar, Punjab, India., Department of Computer Science and Engineering, Chandigarh University, Mohali, Punjab, India., School of Computer Science and Engineering, SCE Taylor's University, Subang Jaya, Malaysia., Graduate School, Duy Tan University, Da Nang, Viet Nam., Department of Mathematics, Faculty of Science, Mansoura University, Mansoura, Egypt., Department of Computer Science and Engineering, Soonchunhyang University, Asan, Korea.

Abstract:  Compression at a very low bit rate(≤0.5bpp) causes degradation in video frames with standard decoding algorithms like H.261, H.262, H.264, and MPEG-1 and MPEG-4, which itself produces lots of artifacts. This paper focuses on an efficient pre-and post-processing technique (PP-AFT) to address and rectify the problems of quantization error, ringing, blocking artifact, and flickering effect, which significantly degrade the visual quality of video frames. The PP-AFT method differentiates the blocked images or frames using activity function into different regions and developed adaptive filters as per the classified region. The designed process also introduces an adaptive flicker extraction and removal method and a 2-D filter to remove ringing effects in edge regions. The PP-AFT technique is implemented on various videos, and results are compared with different existing techniques using performance metrics like PSNR-B, MSSIM, and GBIM. Simulation results show significant improvement in the subjective quality of different video frames. The proposed method outperforms state-of-the-art de-blocking methods in terms of PSNR-B with average value lying between (0.7-1.9db) while (35.83-47.7%) reduced average GBIM keeping MSSIM values very close to the original sequence statistically 0.978. 

Retracted: No

PubPeer comments:
 At least one paragraph of this paper is remarkable for its language.  To lessen calculation intricacy - the term  computational complexity is typically not a subject for word-by-word substitutions.  In the event that ( 8 ) isnu2019t fulfilled, another edge esteem is set to ascertain PV containing ancient rarities which are near the square limit to such an extent that formula  - while I was able to parse  esteem as  value , I struggle to understand what the phrase  ancient rarities stands for. And I have not looked beyond the paragraph containing the above artifacts. At best, copy-editing seems to have gone badly wrong here. ,
Dysregulation of Hypothalamic Gene Expression and the Oxytocinergic System by Soybean Oil Diets in Male Mice
Authors: Ei-Wen Yang
Jack Reid
Matthew Valdez
Jose Martinez-Lomeli
Tao Jiang
Jonathan R Deans
Holly Richardson
Margarita C Curras-Collazo
Frances M Sladek
Catherine Ho
Gwendolyn Gonzalez
Poonamjot Deol
Jane R Evans
Joseph Valdez
Elena Kozlova
Edward Truong
Journal: Endocrinology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Plenish; coconut oil; diabetes; high-fat diet; linoleic acid
Affiliations: Department of Molecular, Cell and Systems Biology, University of California, Riverside, California, Neuroscience Graduate Program, University of California, Riverside, California, Department of Computer Science and Engineering, University of California Riverside, California

Abstract:  Soybean oil consumption has increased greatly in the past half-century and is linked to obesity and diabetes. To test the hypothesis that soybean oil diet alters hypothalamic gene expression in conjunction with metabolic phenotype, we performed RNA sequencing analysis using male mice fed isocaloric, high-fat diets based on conventional soybean oil (high in linoleic acid, LA), a genetically modified, low-LA soybean oil (Plenish), and coconut oil (high in saturated fat, containing no LA). The 2 soybean oil diets had similar but nonidentical effects on the hypothalamic transcriptome, whereas the coconut oil diet had a negligible effect compared to a low-fat control diet. Dysregulated genes were associated with inflammation, neuroendocrine, neurochemical, and insulin signaling. Oxt was the only gene with metabolic, inflammation, and neurological relevance upregulated by both soybean oil diets compared to both control diets. Oxytocin immunoreactivity in the supraoptic and paraventricular nuclei of the hypothalamus was reduced, whereas plasma oxytocin and hypothalamic Oxt were increased. These central and peripheral effects of soybean oil diets were correlated with glucose intolerance but not body weight. Alterations in hypothalamic Oxt and plasma oxytocin were not observed in the coconut oil diet enriched in stigmasterol, a phytosterol found in soybean oil. We postulate that neither stigmasterol nor LA is responsible for effects of soybean oil diets on oxytocin and that Oxt messenger RNA levels could be associated with the diabetic state. Given the ubiquitous presence of soybean oil in the American diet, its observed effects on hypothalamic gene expression could have important public health ramifications. 

Retracted: No

PubPeer comments:
 The first author of this paper is [doling out dietary advice to the public] :  If there s one message I want people to take away, it s this: reduce consumption of soybean oil, Deol said about the most recent study. This is dangerous and unscientific. This study was done in mice. There is nothing in this study that warrants alarming the public in the way this author has. ,
Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke
Authors: Xi Kuang
Jun-Rong Du
Ke Liu
Lu Yu
Chu Chen
Liang-Fen Wang
Hao Zhang
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Ischemic brain injury; neuroinflammatory response; glial activation; neutrophil infiltration; transcription factors
Affiliations: Key Laboratory of Drug Targeting and Drug Delivery Systems of Ministry of Education, Department of Pharmacology, West China School of Pharmacy, Sichuan University "985 Projects - Science and Technology Innovation Platform for Novel Drug Development and Translational Neuroscience Center", Chengdu, China.

Abstract:  Background: Ischemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration. Transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) contribute to ischemic neuroinflammatory processes and secondary brain injury by releasing proinflammatory mediators. Kaempferol-3-O-rutinoside (KRS) and kaempferol-3-O- glucoside (KGS) are primary flavonoids found in Carthamus tinctorius L. Recent studies demonstrated that KRS protected against ischemic brain injury. However, little is known about the underlying mechanisms. Flavonoids have been reported to have antiinflammatory properties. Herein, we explored the effects of KRS and KGS in a transient focal stroke model. Methodology/principal findings: Rats were subjected to middle cerebral artery occlusion for 2 hours followed by 22 h reperfusion. An equimolar dose of KRS or KGS was administered i.v. at the beginning of reperfusion. The results showed that KRS or KGS significantly attenuated the neurological deficits, brain infarct volume, and neuron and axon injury, reflected by the upregulation of neuronal nuclear antigen-positive neurons and downregulation of amyloid precursor protein immunoreactivity in the ipsilateral ischemic hemisphere. Moreover, KRS and KGS inhibited the expression of OX-42, glial fibrillary acidic protein, phosphorylated STAT3 and NF-κB p65, and the nuclear content of NF-κB p65. Subsequently, these flavonoids inhibited the expression of tumor necrosis factor α, interleukin 1β, intercellular adhesion molecule 1, matrix metallopeptidase 9, inducible nitric oxide synthase, and myeloperoxidase. Conclusion/significance: Our findings suggest that postischemic treatment with KRS or KGS prevents ischemic brain injury and neuroinflammation by inhibition of STAT3 and NF-κB activation and has the therapeutic potential for the neuroinflammation-related diseases, such as ischemic stroke. 

Retracted: No

PubPeer comments:
 Figure 3D appears to have an overlap between 2 images ![file] , 
 Two overlaps can be seen in Figure 2D and Figure 4C D. One of the overlaps was seen in three images, involving a flip, all marked with boxes with same color ![file] ,
High lncRNA MEG3 expression is associated with high mortality rates in patients with sepsis and increased lipopolysaccharide‑induced renal epithelial cell and cardiomyocyte apoptosis
Authors: Weiming Xu
Ye Jin
Xiaojun Shi
Kang Chen
Qing Shen
Feng Wang
Journal: Experimental and Therapeutic Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: cardiomyocytes; long non-coding RNA maternally expressed 3; renal epithelial cell; sepsis.
Affiliations: Department of Emergency Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 201400, P.R. China.

Abstract:  Long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) has been reported to be a key component in cancer biology. Preliminary microarray data from a previous study indicated that lncRNA MEG3 expression was altered in plasma of patients with sepsis. The present study found that the plasma levels of lncRNA MEG3 were significantly higher in sepsis patients compared with healthy controls. Patients were subsequently divided into high and low lncRNA MEG3 expression groups according to the Youden's index. Patients from the high lncRNA MEG3 expression group exhibited a significantly higher mortality rate compared with those from the low lncRNA MEG3 expression group. According to treatment outcomes, patients were divided into survival and mortality groups. It was observed that the pre-therapy expression levels of lncRNA MEG3 were significantly higher in mortality group compared with the survival group. Cell experiments in vitro revealed that lncRNA MEG3 overexpression and silencing using siRNA promoted and inhibited renal epithelial cell and cardiomyocyte apoptosis induced by lipopolysaccharide, respectively. In conclusion, these data suggest that lncRNA MEG3 overexpression may be involved in sepsis, and the downregulation of lncRNA MEG3 may serve as a potential therapeutic target for sepsis. 

Retracted: No

PubPeer comments:
 Figure 4.  Following LPS treatment, LncRNA MEG3 overexpression resulted in significantly increased apoptosis, whereas lncRNA MEG3 knockdown by siRNA significantly inhibited apoptosis in (A) renal epithelial cells and (B) AC12 cardiomyocytes. High similarity between C and NC panels in 4A. Could the authors check that the same data-file has not been plotted twice by mistake? ![file] ,
CRISPR-Cas9 mediated efficient PD-1 disruption on human primary T cells from cancer patients
Authors: Lianru Zhang
Huizi Sha
Baorui Liu
Lixia Yu
Juan Du
Jiankui Zhou
Bin Shen
Fangjun Chen
Jie Shao
Shu Su
Bian Hu
Lei Cheng
Yinan Du
Fanyan Meng
Zhengyun Zou
Xingxu Huang
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: T cells; PD-L1; PD-1; gene knockout; electroporation
Affiliations: The Comprehensive Cancer Centre of Drum Tower Hospital, Medical School of Nanjing University &Clinical Cancer Institute of Nanjing University, Nanjing 210008, China., MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center of Nanjing University, National Resource Center for Mutant Mice, Nanjing 210061, China., State Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing 210029, China., School of Life Science and Technology, ShanghaiTech University, 100 Haike Rd., Pudong New Area, Shanghai 201210, China.

Abstract:  Strategies that enhance the function of T cells are critical for immunotherapy. One negative regulator of T-cell activity is ligand PD-L1, which is expressed on dentritic cells (DCs) or some tumor cells, and functions through binding of programmed death-1 (PD-1) receptor on activated T cells. Here we described for the first time a non-viral mediated approach to reprogram primary human T cells by disruption of PD-1. We showed that the gene knockout of PD-1 by electroporation of plasmids encoding sgRNA and Cas9 was technically feasible. The disruption of inhibitory checkpoint gene PD-1 resulted in significant reduction of PD-1 expression but didn't affect the viability of primary human T cells during the prolonged in vitro culture. Cellular immune response of the gene modified T cells was characterized by up-regulated IFN-γ production and enhanced cytotoxicity. These results suggest that we have demonstrated an approach for efficient checkpoint inhibitor disruption in T cells, providing a new strategy for targeting checkpoint inhibitors, which could potentialy be useful to improve the efficacy of T-cell based adoptive therapies. 

Retracted: No

PubPeer comments:
 Could the authors go into detail about the software and hardware used to process and plot these NMR patterns?. ![file] , 
 Could the authors comment on what appear to be some repeated features? Fig. 11. 1 H-NMR spectra of probe NIRM, probe NIRM with Hg2+ and control compound NIC. ![file] , 
 #2 The NIRM only trace has issues as well. ![file] What happed at 7.5 ppm? ![file] What happened at ppm 8? ![file] , 
 Panels in Figures 12 and 7 of both papers also look very similar. Could the authors please clarify if these are the exact same materials? The paper does not appear to be listed in the references of this paper. ![file] ![file] , 
 #4 Here adjusting the contrast and brightness of Fig 12 to clarify the contrast with [Angamuthu et al (2018)] . ![file] ,
Dissociation of cardiogenic and postnatal myocardial activities of GATA4
Authors: Branko V Latinkić
Emmanuel Roy
Joseph M Gallagher
Mona Nemer
Hiba Komati
Journal: Molecular and Cellular Biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GATA4; transcription factor; cardiogenesis; cardiomyocyte survival; transcriptional synergy
Affiliations: School of Biosciences, Cardiff University, Cardiff, United Kingdom., Laboratory of Cardiac Development and Differentiation, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario, Canada, Graduate Program in Biomedical Sciences, University of Montréal, Montréal, Québec, Canada, School of Biosciences, Cardiff University, Museum Avenue, Cardiff, United Kingdom

Abstract:  Transcription factor GATA4 is a critical regulator of the embryonic and postnatal heart, but the mechanisms and cofactors required for its diverse functions are not fully understood. Here, we show that whereas the N-terminal domain of GATA4 is required for inducing cardiogenesis and for promoting postnatal cardiomyocyte survival, distinct residues and domains therein are necessary to mediate these effects. Cardiogenic activity of GATA4 requires a 24-amino-acid (aa) region (aa 129 to 152) which is needed for transcriptional synergy and physical interaction with BAF60c. The same region is not essential for induction of endoderm or blood cell markers by GATA4, suggesting that it acts as a cell-type-specific transcriptional activation domain. On the other hand, a serine residue at position 105, which is a known target for mitogen-activated protein kinase (MAPK) phosphorylation, is necessary for GATA4-dependent cardiac myocyte survival and hypertrophy but is entirely dispensable for GATA4-induced cardiogenesis. We find that S105 is differentially required for transcriptional synergy between GATA4 and serum response factor (SRF) but not other cardiac cofactors such as TBX5 and NKX2.5. The findings provide new insight into GATA4 mechanisms of action and suggest that distinct regulatory pathways regulate activities of GATA4 in embryonic development and postnatal hearts. 

Retracted: No

PubPeer comments:
 This paper was part of a structured search into possible cases of image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long Figure 4B: * Red lines: Three lanes appear to share similarities. ![file] Figure 6B: * Red boxes: two bands appear to look similar. ![file] The journal did not take any action. Could the authors perhaps take away any concern by posting the original blots here? ,
Antagonism of RIP1 using necrostatin-1 (Nec-1) ameliorated damage and inflammation of HBV X protein (HBx) in human normal hepatocytes
Authors: Yongjie Huang
Linsen Xie
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: HBx; NF-κB; RIP1; inflammation; necrostatin-1.
Affiliations: Department of Clinical Laboratory, Zhengzhou Central Hospital Affiliated To Zhengzhou University, Zhengzhou, China

Abstract:  Hepatitis B virus X protein (HBx), encoded by the hepatitis B virus (HBV) genome, plays a pivotal in mediating pathogenicity in liver diseases. However, the underlying mechanisms are still needed to be elucidated. Receptor-interacting protein 1 (RIP1) has been identified as a serine/threonine kinase with various biological functions in cell fate, proliferation, and death. In the current study, we found that overexpression of HBx in LO2 human normal hepatocytes increased the expression of RIP1. Importantly, our results indicate that blockage of RIP1 using its specific antagonist necrostatin-1 (Nec-1) ameliorated HBx-induced oxidative stress by mitigating the production of ROS and Nox-4 expression. Also, the presence of Nec-1 improved HBx-induced mitochondrial dysfunction by increasing MMP. Importantly, we found that Nec-1 could inhibit the production of pro-inflammatory cytokines IL-6, IL-8, and CXCL2 as well as the secretion of HMGB1. Mechanistically, we found that Nec-1 treatment suppressed the activation of the JNK/AP-1 and NF-κB signalling pathways. Our findings implicated a novel biological function of RIP1 in HBx-induced cytotoxicity and inflammation in human normal hepatocytes. Antagonism of RIP1 might be a potential therapeutic approach for the treatment of HBV-associated liver diseases. 

Retracted: No

PubPeer comments:
 This work is one of two by the authors that appear to duplicate certain crucial images: 1. Bahmani, S.H., Huat, B.B., Asadi, A. and Farzadnia, N., 2014. Stabilization of residual soil using SiO2 nanoparticles and cement. Construction and Building Materials, 64, pp.350-359. 2. Bahmani, S.H., Farzadnia, N., Asadi, A. and Huat, B.B., 2016. The effect of size and replacement content of nanosilica on strength development of cement treated residual soil. Construction and Building Materials, 118, pp.294-306. The image below shows the relevant duplication. Highlighted in red is an image that was presented in both papers, but which was turned upside-down (presumably in order to disguise the connection). As far as I can tell, the image reportedly did represent the same material. However, its scale bar and associated information were manipulated between the two papers. Highlighted in blue is an image that was represented twice in Paper 2, reportedly representing two different materials. The images even share an identical timestamp. Highlighted in orange are two distinct images of the same site, reportedly representing two different materials. The scale and aspect ratio differed between the two images, but they are unmistakably of the same site. ![file] ,
<p>DICER1-AS1 Promotes the Malignant Behaviors of Colorectal Cancer Cells by Regulating miR-296-5p/STAT3 Axis</p>
Authors: Shuhong Liu
Ning Ma
Chuanyu Ma
Chuanna Miao
Lili Qin
Minglei Luo
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: CRC; DICER1-AS1; metastasis; miR-296-5p; proliferation.
Affiliations: Department of Proctology, Linyi Central Hospital, Linyi, Shandong Province, People's Republic of China., Department of Radiotherapy, Linyi Cancer Hospital, Linyi, Shandong Province, People's Republic of China.

Abstract:  Background: Long non-coding RNA (lncRNA) exerts a regulatory role in the occurrence and progression of tumors. This study aimed at probing into the function and mechanism of lncRNA DICER1 antisense RNA 1 (DICER1-AS1) in colorectal cancer (CRC). Methods: The expressions of DICER1-AS1, miR-296-5p and STAT3 mRNA were tested by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was employed to detect cell proliferation, and Transwell was used to detect cell migration and invasion. In addition, the expressions of apoptosis-related proteins Bax and Bcl2 were detected by Western blot. Interactions between DICER1-AS1 and miR-296-5p, and miR-296-5p and STAT3 were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. Results: The expressions of DICER1-AS1 and STAT3 mRNA were significantly up-regulated while miR-296-5p expression was remarkably down-regulated in CRC tissues and cell lines. Over-expression of DICER1-AS1 or transfection of miR-296-5p inhibitors could promote the proliferation, migration and invasion and inhibit apoptosis of CRC cells, whereas knockdown of DICER1-AS1 or transfection of miR-296-5p mimics had the opposite effects. Additionally, DICER1-AS1 could down-regulate miR-296-5p expression via sponging it. DICER1-AS1 also enhanced the expression of STAT3, which was identified as a target gene of miR-296-5p. Conclusion: DICER1-AS1 acts as an oncogenic lncRNA in CRC via modulating miR-296-5p/STAT3 axis. Our results provide a new direction for the diagnosis and treatment of CRC. 

Retracted: No

PubPeer comments:
 The method for measuring mature miR-296-5p would not work as described. A standard reverse transcription kit will not prepare mature miRNAs for amplification. Instead, a microRNA-specific RT strategy would be needed, specifically in this case a stem-loop RT primer strategy, as reflected in the  forward primer described in the methods section. However, the  forward and  reverse primers also appear to have been switched, a feature shared with numerous other articles claiming to amplify mature miR-296-5p. The absence of apparent understanding that miRNAs must be RT d and amplified differently from other RNAs diminishes confidence in the miRNA portions of the paper. ,
Multifunctional Fe3O4@nSiO2@mSiO2–Fe core–shell microspheres for highly efficient removal of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT) from aqueous media
Authors: Junhui He
Hua Tian
Feng Liu
Journal: Journal of Colloid and Interface Science (2014)
Discipline: CHEMISTRY
Keywords: Catalytic dechlorination; Core–shell structure; DDT; Magnetic separation; Mesoporous silica.

Abstract:  A novel multifunctional microsphere with an iron oxide-improved mesoporous silica shell and a Fe3O4@SiO2 core has been successfully prepared by a hydrothermal method and impregnation process. The resulting Fe3O4@nSiO2@mSiO2-Fe core-shell microspheres are utilized as a catalyst for the removal of 1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane (DDT) and its derivatives, i.e., 1,1-dichloro-2,2-bis(4-chlorophenyl) ethane (DDD) and 1,1-dichloro-2,2-bis(4-chlorophenyl) ethylene (DDE). The results indicated that the iron oxide nanoparticles were well dispersed on the mesoporous silica shell of Fe3O4@nSiO2@mSiO2. DDT, DDD and DDE could be quickly and effectively removed from aqueous media in 60 min, and completely dechlorinated at 350°C by Fe3O4@nSiO2@mSiO2-Fe. More importantly, the Fe3O4@nSiO2@mSiO2-Fe microspheres were superparamagnetic and could be separated and collected easily and rapidly using a magnet. 

Retracted: No

PubPeer comments:
 Figure 1 shows two identical XRD for different samples. ![file] ,