PReD-Bench/PRed-Bench huggingface dataset:
GRHL2 inhibits colorectal cancer progression and metastasis via oppressing epithelial-mesenchymal transition
Authors: Yingjun Quan
Zhou Yang
Zhijun Min
Yusheng Chen
Dejun Wu
Journal: Cancer Biology & Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: Grainyhead-like 2; ZEB1; colorectal cancer; epithelial-mesenchymal transition; mesenchymal-epithelial transition.
Affiliations: Department of General Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center , Shanghai , China.

Abstract:  Our previous study has demonstrated that knockdown of Grainyhead-like 2(GRHL2) in colorectal cancer (CRC) cells inhibited cell proliferation by targeting ZEB1. This study aimed at researching whether knockdown of GRHL2 promoted CRC progression and metastasis via inducing epithelial-mesenchymal transition (EMT). GRHL2-upregulated SW-620/GRHL2+ and GRHL2-knockdown HCT116/GRHL2-KD, HT29/GRHL2-KD cells and their control cells were generated. The morphological changes after overexpression and knockdown GRHL2 were observed. qRT-PCR, Western blotting, and Immunofluorescence were used to detect EMT markers: E-cadherin, Vimentin, p-catein, ZO-1 and ZEB1 expression. Then, sh-ZEB1 was transfected to GRHL2 knockdown cells to research the relationship between GRHL2 and ZEB1. Transwell and wound healing assays were further performed to detect the impact of GRHL2 on invasion and migration in vitro. CRC cells were injected into mice tail vein to verify the impact of GRHL2 on CRC metastasis. Morphological change of mesenchymal-epithelial transition (MET) could be observed in SW620/GRHL2+ cell. The expression of epithelial markers: E-cadherin, β-catenin, ZO-1 were up-regulated, while mesenchymal markers: Vimentin was decreased. Meanwhile, opposite EMT morphological change could be observed in HCT116/GRHL2-KD cell, accompanied by reverse change of E-cadherin, β-catenin, ZO-1, and Vimentin. The expression level of GRHL2 and ZEB1 was found negative in both SW620/GRHL2+ and HCT116/GRHL2-KD cells. Knockdown of ZEB1 by siRNA in HCT116/GRHL2-KD and HT29/GRHL2-KD could upregulate expression of E-cadherin and GRHL2. GRHL2 knockdown also promoted migration, invasion in vitro and CRC metastasis in mice model. In conclusion, GRHL2/ZEB1 axis inhibits CRC progression and metastasis via oppressing EMT. 

Retracted: No

PubPeer comments:
 Figure 6 appears to have (partially) duplicated images. 6B is hard to see, but it appears the image coloring has been adjusted. I ve tried to match the coloring as best as I could in an image I added next to the one in the top row. ![file] ,
The siRNA silencing of DcR3 expression induces Fas ligand-mediated apoptosis in HepG2 cells
Authors: Tuanjie Zhao
Shulin Ren
Xiaona Zhou
Yingchen Xu
Chaojie Liang
Jixiang Wu
Journal: Experimental and Therapeutic Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: Fas ligand; HepG2; apoptosis; decoy receptor 3; small interfering RNA.
Affiliations: Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, P.R. China.

Abstract:  Dysfunctional Fas ligand (FasL) may inhibit the apoptosis of tumor cells. FasL contains two receptors, Fas and Decoy Receptor 3 (DcR3). DcR3 competitively binds to FasL over Fas, resulting in the inhibition of FasL-mediated apoptosis. Therefore, it was suggested that the downregulation of DcR3 expression enhances FasL-mediated apoptosis. In the current study, the expression of DcR3 was silenced in liver cancer HepG2 cells in order to study the effect of FasL on HepG2 cell activity and invasiveness. DcR3 siRNA knockdown HepG2 cells (KD), DcR3 blank plasmid control HepG2 cells and wild-type HepG2 cells (WT) were treated with FasL (10 ng/ml). Flow cytometry was used to detect changes in the cell cycle and apoptosis. MTS, clonogenic, wound healing and Transwell assays were performed to examine changes in cell activity, proliferation, migration and invasiveness. Reverse transcription polymerase chain reaction and western blot analysis were performed to measure the expression of DcR3, matrix metallopeptidase 9 (MMP9), vascular endothelial growth factor (VEGF)-C and VEGF-D. The results demonstrated that, compared with WT cells, the proportion of KD cells in the G2/M phase decreased following treatment with FasL. KD cells were more sensitive to FasL-induced apoptosis. Following treatment with FasL, the activity and proliferation, migration and invasion of KD cells were reduced, and the expression of MMP9, VEGF-C and VEGF-D decreased. Furthermore, it was demonstrated that DcR3 is involved in the proliferation and invasion of HepG2 cells, and this mechanism may be associated with the regulatory effect of the expression of MMP9, VEGF-C and VEGF-D; however, the exact mechanism of action remains unclear. FollowingDcR3 silencing, FasL-mediated apoptosis increased in HepG2 cells. Therefore, DcR3 combined with FasL may be a potential target for the treatment of liver cancer. 

Retracted: No

PubPeer comments:
 Figure 2 appears to have some overlapping images after rotation, flipping and or brightness adjustment. There could be more. Difficult to understand how this could be due to errors during figure assembly. *** ![file] ,
MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-β1 signaling pathway
Authors: R Jing
Q-Q Zhong
T-Y Long
J-W Zhang
W Pan
Z-X Qian
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-808; cardiomyocyte apoptosis; caspase-3; caspase-9; myocardial infarction
Affiliations: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing Key Laboratory of Precision Medicine of Coronary Atherosclerotic Disease, Clinical Center for Coronary Heart Disease, Capital Medical University, Beijing, China. .

Abstract:  Objective: To investigate the effects of micro ribonucleic acid (miR)-808 on cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction (MI) by regulating the transforming growth factor-β1 (TGF-β1) signaling pathway. Materials and methods: A total of 24 specific pathogen-free female Sprague-Dawley rats were enrolled and randomly divided into normal group, model group, and miR-808 group, 8 rats in each group. In the model group and miR-808 group, MI model was prepared by ligation of the left anterior descending coronary artery in the rats. The miR-808 group was transfected with miR-808 lentivirus after the model was established. After one week of intervention, the expression of TGF-β1 was detected by reverse transcription-polymerase chain reaction (RT-PCR). The cardiac function of rats was determined by echocardiography. The myocardium of rats was observed by Masson staining. The cardiomyocyte apoptosis of rats was examined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The expression levels of caspase-3 and caspase-9 were detected by Western blotting. Results: The expression of TGF-β1 mRNA was higher in the model group than that in the normal group (p&lt;0.05), but compared with that in the model group, it was lower in the miR-808 group. The myocardial function and cardiomyocyte survival rate in the miR-808 group was better and higher than those in the model group (p&lt;0.05). The expression levels of caspase-3 and caspase-9 in the miR-808 group were lower than those in the model group (p&lt;0.05). Conclusions: MiR-808 can inhibit cardiomyocyte apoptosis in rats with MI by down-regulating TGF-β1 expression and inhibiting the expressions of caspase-3 and caspase-9. 

Retracted: No

PubPeer comments:
 Multiple figures in this publication contain duplicated elements. In particular, this panel in Figure 2: ![file] And every panel in Figure 4: ![file] , 
 #1 ![file] , 
 #1 I am beginning to see what Oxalis Capillacea means about  multiple figures . ![file] , 
 #1 thx for point out. after we recheck our primary datauff0cit just showed like that. ,
Association of tapasin and COPI provides a mechanism for the retrograde transport of major histocompatibility complex (MHC) class I molecules from the Golgi complex to the endoplasmic reticulum
Authors: Hans-Olov Sjogren
Ping Wang
Suling Li
Marc Jevon
Shangwu Chen
Janice Griffith
Per O Anderson
Monique J Kleijmeer
Kajsa M Paulsson
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Tapasin; COPI coatomer; MHC class I; TAP; antigen processing
Affiliations: Institution of Tumor Immunology, Lund University, Solvegatan 21, s-223 62 Lund, Sweden.

Abstract:  Tapasin is a subunit of the transporter associated with antigen processing (TAP). It associates with the major histocompatibility complex (MHC) class I. We show that tapasin interacts with beta- and gamma-subunits of COPI coatomer. COPI retrieves membrane proteins from the Golgi network back to the endoplasmic reticulum (ER). The COPI subunit-associated tapasin also interacts with MHC class I molecules suggesting that tapasin acts as the cargo receptor for packing MHC class I molecules as cargo proteins into COPI-coated vesicles. In tapasin mutant cells, neither TAP nor MHC class I are detected in association with the COPI coatomer. Interestingly, tapasin-associated MHC class I molecules are antigenic peptide-receptive and detected in both the ER and the Golgi. Our data suggest that tapasin is required for the COPI vesicle-mediated retrograde transport of immature MHC class I molecules from the Golgi network to the ER. 

Retracted: No

PubPeer comments:
 The Western bolt bands of u03b3-COPI (red box) and Tapasin (blue box) in FIG 1 were reused in FIG 3B. ![file] ,
GE11 peptide conjugated selenium nanoparticles for EGFR targeted oridonin delivery to achieve enhanced anticancer efficacy by inhibiting EGFR-mediated PI3K/AKT and Ras/Raf/MEK/ERK pathways
Authors: Jiye Cai
Jiang Pi
Hua Jin
Huaihong Cai
Peihui Yang
Fen Yang
Zheng W Chen
Jinhuan Jiang
Journal: Drug Delivery (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: EGFR targeting; GE11 peptide; Selenium nanoparticles; delivery; oridonin.
Affiliations: State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, PR China;, Department of Chemistry, Jinan University, Guangzhou, PR China, Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL, USA;

Abstract:  Selenium nanoparticles (Se NPs) have attracted increasing interest in recent decades because of their anticancer, immunoregulation, and drug carrier functions. In this study, GE11 peptide-conjugated Se NPs (GE11-Se NPs), a nanosystem targeting EGFR over-expressed cancer cells, were synthesized for oridonin delivery to achieve enhanced anticancer efficacy. Oridonin loaded and GE11 peptide conjugated Se NPs (GE11-Ori-Se NPs) were found to show enhanced cellular uptake in cancer cells, which resulted in enhanced cancer inhibition against cancer cells and reduced toxicity against normal cells. After accumulation into the lysosomes of cancer cells and increase of oridonin release under acid condition, GE11-Ori-Se NPs were further transported into cytoplasm after the damage of lysosomal membrane integrity. GE11-Ori-Se NPs were found to induce cancer cell apoptosis by inducting reactive oxygen species (ROS) production, activating mitochondria-dependent pathway, inhibiting EGFR-mediated PI3K/AKT and inhibiting Ras/Raf/MEK/ERK pathways. GE11-Se NPs were also found to show active targeting effects against the tumor tissue in esophageal cancer bearing mice. And in nude mice xenograft model, GE11-Ori-Se NPs significantly inhibited the tumor growth via inhibition of tumor angiogenesis by reducing the angiogenesis-marker CD31 and activation of the immune system by enhancing IL-2 and TNF-α production. The selenium contents in mice were found to accumulate into liver, tumor, and kidney, but showed no significant toxicity against liver and kidney. This cancer-targeted design of Se NPs provides a new strategy for synergistic treating of cancer with higher efficacy and reduced side effects, introducing GE11-Ori-Se NPs as a candidate for further evaluation as a chemotherapeutic agent for EGFR over-expressed esophageal cancers. 

Retracted: No

PubPeer comments:
 The authors may wish to check Fig 10. Here, row A: ![file] Row D: ![file] ,
LncRNA SNHG15 promotes proliferation and migration of lung cancer via targeting microRNA-211-3p
Authors: Z-L Zhang
K Liu
J Liu
M-Y Zhang
H-X Cui
L Fu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; SNHG15; lung cancer; microRNA-211-3p; proliferation
Affiliations: Department of Thoracic Surgery, Affiliated Hospital of Weifang Medical University, Weifang, China. .

Abstract:  Objective: To investigate whether lncRNA (long non-coding RNA) SNHG15 could regulate the proliferation and migration of lung cancer via microRNA-211-3p and its underlying mechanism. Patients and methods: SNHG15 expression in 55 LC (lung cancer) tissues and 30 normal lung tissues was detected by qRT-PCR (quantitative Real Time-Polymerase Chain Reaction). The relationship between SNHG15 expression and pathological characteristics of LC patients was analyzed the by Kaplan-Meier method. The target microRNA of SNHG15 was predicted by bioinformatics and verified by dual-luciferase reporter gene assay. Viability, cell cycle and migration of LC cells after altering expressions of SNHG15 or microRNA-211-3p were detected by cell counting kit-8 (CCK-8), flow cytometry and transwell assay, respectively. Results: SNHG15 was highly expressed in LC tissues than that of normal lung tissues. Besides, LC patients with stage I-II presented lower expression of SNHG15 than those with stage III-IV. SNHG15 expression was correlated to tumor size, TNM stage, and lymph node metastasis, whereas not correlated to age and sex of LC patients. For in vitro studies, SNHG15 knockdown resulted in viability reduction, cell cycle arrest and reduced migration of LC cells, which were reversed by the microRNA-211-3p knockdown. Conclusions: SNHG15 is highly expressed in LC tissues, which promotes the occurrence and progression of LC via regulating proliferation and migration of LC cells by targeting microRNA-211-3p. 

Retracted: No

PubPeer comments:
  LC tissues and paracancerous tissues in LC patients undergoing radical resection of pulmonary carcinoma in Affiliated Hospital of Weifang Medical University from **April 2012 year to July 2017 year** were surgically resected. Fig 1C:  The LC patients with higher expression of SNHG15 presented shorter overall survival compared with those with lower expression . ![file] It appears that when this paper was published in mid-2018, patient survival had been tracked through 80 months, i.e. to dates ranging from **December 2018 to March 2024**. Is that correct? ,
KDM4B promotes gastric cancer metastasis by regulating miR‐125b‐mediated activation of Wnt signaling
Authors: Zhen Feng
Jin Ling Yu
Jia-Chen Jing
Shao-Ying Wang
Nan Tang
Zhong-Hua Chen
Jing Hong
Bei-Na Ji
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: KDM4B; Wnt; gastric cancer; metastasis; miR-125b.
Affiliations: Department of Gastroenterology, Xu Hui District Center Hospital, Shanghai, China.

Abstract:  Emerging evidence has demonstrated that the aberrant expression of histone-modifying enzymes such as histone demethylases contributes to gastric carcinogenesis and progression. The role of KDM4B in cancer progression has been gradually revealed. However, the underlying mechanisms regulating gastric cancer metastasis of KDM4B remain unclear. In the present study we determined KDM4B expression in gastric cancer and its biologic function in vitro and in vivo. We found that KDM4B expression was significantly increased in most gastric cancer tissues compared with the adjacent normal tissues. Upregulated expression of KDM4B in human gastric cancer was correlated with poor prognosis. In vitro, KDM4B overexpression in AGS cells promoted cell invasion, whereas knockdown of KDM4B inhibited cell invasion. Furthermore, KDM4B overexpression also promoted tumor metastasis in vivo. Mechanistically, KDM4B upregulated miR-125b expression and activated Wnt signaling pathway. More important, miR-125b partially mediated KDM4B-induced activation of Wnt signaling. Finally, we demonstrated that KDM4B promoted gastric cancer cell invasion in vitro and cancer metastasis in vivo, at least in part, by upregulating miR-125b expression. These data provided novel insights on the role of KDM4B-driven gastric cancer metastasis and indicated that KDM4B may be served as a potential target for gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have one flipped the rightmost image and added cells (red circles) to get the middle image. I also noticed a duplication within that image (circled in orange) ![file] ,
T helper cell subpopulations repertoire in peripheral blood and its correlation with sex of newly diagnosed arthritis patients: A gender based study
Authors: Shagufta Moin
Haris Saeed
Mohammad Owais
Abdul Qayyum Khan
Somaiya Mateen
Journal: International Immunopharmacology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Autoimmunity; Human study; Newly diagnosed patients; Pro-inflammatory cytokines; Rheumatoid arthritis
Affiliations: Department of Biochemistry, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh 202002, India., Molecular Immunology Laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, Uttar Pradesh 202002, India., Department of Orthopaedic Surgery, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India., Molecular Immunology Laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, Uttar Pradesh 202002, India. Electronic address: .

Abstract:  Rheumatoid arthritis (RA) is an inflammatory autoimmune disorder. Autoreactive T cells play a very significant role in the pathogenesis of RA. However, the exact mechanisms of disease severity and pathogenesis are poorly understood. We attempted to correlate T-helper cell activities with sexes of newly diagnosed patients with RA. The patients were divided based on their sex and disease severity. Examination of the expression of various factors using quantitative real-time PCR and FACS analysis of peripheral blood mononuclear cells revealed that T-bet, ROR-γt, Foxp3, and the level of cytokines associated with Th1 cells were almost identical among male and female patients with RA. Interestingly, there was a high correlation between Th17 expression and disease severity in female patients with RA. In general, there was no significant correlation between Th1 cell population and the disease severity in newly diagnosed patients with RA. In contrast, the frequency of both Th17 and Treg cells was higher in patients with more severe disease. The results suggested that, in patients with RA, the T-helper cell balance within peripheral blood was skewed towards the Th17 and Treg phenotypes. Besides Th17- and Treg-associated cytokines, elevated expression of IL-27/IL-23 cytokines might also be responsible for increased disease severity in female patients with RA. 

Retracted: No

PubPeer comments:
 Figure 2. The Control (F) panel in A and the Control panel in B appear to show similar constellations of dots. Yet they are presented as different experiments with some differences in the upper quadrants and differently gated percentages. Could the authors please clarify? ![file] ,
Deep learning for inferring gene relationships from single-cell expression data
Authors: Ye Yuan
Ziv Bar-Joseph
Journal: Proceedings of the National Academy of Sciences of the United States of America (2019)
Discipline: Multidisciplinary
Keywords: causality inference; deep learning; gene interactions.
Affiliations: Machine Learning Department, School of Computer Science, Carnegie Mellon University, Pittsburgh, PA 15213., Machine Learning Department, School of Computer Science, Carnegie Mellon University, Pittsburgh, PA 15213; ., Computational Biology Department, School of Computer Science, Carnegie Mellon University, Pittsburgh, PA 15213.

Abstract:  Several methods were developed to mine gene-gene relationships from expression data. Examples include correlation and mutual information methods for coexpression analysis, clustering and undirected graphical models for functional assignments, and directed graphical models for pathway reconstruction. Using an encoding for gene expression data, followed by deep neural networks analysis, we present a framework that can successfully address all of these diverse tasks. We show that our method, convolutional neural network for coexpression (CNNC), improves upon prior methods in tasks ranging from predicting transcription factor targets to identifying disease-related genes to causality inference. CNNC's encoding provides insights about some of the decisions it makes and their biological basis. CNNC is flexible and can easily be extended to integrate additional types of genomics data, leading to further improvements in its performance. 

Retracted: No

PubPeer comments:
 There are a few points in the paper where there is a minor error, since GSEA is a method and not a database of gene lists (which I think most commonly would be MSigDB). **Using CNNC for Functional Assignments (Results):**  *For each of these functions, we obtained known genes from gene set enrichment analysis (**GSEA**) (30) and trained CNNC using all expression data on 2 3 of these genes holding the other 1 3 as a test set.* **Known Genes for Functional Assignment Testing (Methods):**  *We downloaded 855 (332, 103, 182, 59, 128) human cell cycle (immune system, rhythm, asthma, COPD, HNC) genes from **GSEA** [u201cMalacardsu201d (31) (a human disease website, https: www.malacards.org )].* **Function assignment : Function assignment train and test data generation (Supplemental Methods):**  *Here we take cell cycle, asthma and COPD as examples. We downloaded 855 (182, 59) human cell cycle (asthma, COPD) genes from **GSEA**(8) (u2018Malacardsu2019 (a human disease website, https: www.malacards.org ), u2018Malacardsu2019) website (9), among which the overlap with mouse gene expression dataset is 682 (147,47) genes.* The corresponding author was kind enough to provide a prompt response to confirm that was MSigDB used (which was downloaded from the GSEA website). So, at least in the interests of encouraging others to list the specific versions of the gene sets used (and providing a more specific MSigDB ciation, if possible), I thought that this should be noted in some way. ,
Thoracic aortic disease in tuberous sclerosis complex: molecular pathogenesis and potential therapies in Tsc2+/− mice
Authors: Limin Gong
Dianna M Milewicz
Dong-chuan Guo
Jiumei Cao
Anthony Estrera
Callie S Kwartler
Hazim Safi
Michael J Gambello
Ulrike Mietzsch
Shao-Qing Kuang
Journal: Human Molecular Genetics (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tuberous sclerosis complex; TSC; aneurysms; aortic; smooth muscle cell
Affiliations: Department of Internal Medicine, University of Texas Medical School at Houston, Houston, TX 77030, USA.

Abstract:  Tuberous sclerosis complex (TSC) is a genetic disorder with pleiotropic manifestations caused by heterozygous mutations in either TSC1 or TSC2. One of the less investigated complications of TSC is the formation of aneurysms of the descending aorta, which are characterized on pathologic examination by smooth muscle cell (SMC) proliferation in the aortic media. SMCs were explanted from Tsc2(+/-) mice to investigate the pathogenesis of aortic aneurysms caused by TSC2 mutations. Tsc2(+/-) SMCs demonstrated increased phosphorylation of mammalian target of rapamycin (mTOR), S6 and p70S6K and increased proliferation rates compared with wild-type (WT) SMCs. Tsc2(+/-) SMCs also had reduced expression of SMC contractile proteins compared with WT SMCs. An inhibitor of mTOR signaling, rapamycin, decreased SMC proliferation and increased contractile protein expression in the Tsc2(+/-) SMCs to levels similar to WT SMCs. Exposure to alpha-elastin fragments also decreased proliferation of Tsc2(+/-) SMCs and increased levels of p27(kip1), but failed to increase expression of contractile proteins. In response to artery injury using a carotid artery ligation model, Tsc2(+/-) mice significantly increased neointima formation compared with the control mice, and the neointima formation was inhibited by treatment with rapamycin. These results demonstrate that Tsc2 haploinsufficiency in SMCs increases proliferation and decreases contractile protein expression and suggest that the increased proliferative potential of the mutant cells may be suppressed in vivo by interaction with elastin. These findings provide insights into the molecular pathogenesis of aortic disease in TSC patients and identify a potential therapeutic target for treatment of this complication of the disease. 

Retracted: No

PubPeer comments:
 Texas is as Texas does. In this era of fake news, Texas officially protects all biomedical research fraud in its universities, as mentioned here https: areomagazine.com 2020 02 20 how-universities-cover-up-scientific-fraud Needless to say, Uncle Sam also fully stands by all fake news published by Texan researchers https: www.govinfo.gov content pkg USCOURTS-ca5-12-20795 pdf USCOURTS-ca5-12-20795-0.pdf In Fig. 5B of this 2010 biomedical research paper emanating from a Texas university, there are lane and gel slice duplications (aided by bits of stretching) in some of them thar Texan ImmunoBlots (TIBs). ![image] ,
Application of Consistency Criteria To Calculate BET Areas of Micro- And Mesoporous Metal-Organic Frameworks
Authors: Randall Q Snurr
Peyman Z Moghadam
Joseph T Hupp
Diego A Gómez-Gualdrón
Omar K Farha
Journal: Journal of the American Chemical Society (2016)
Discipline: CHEMISTRY
Keywords: Metal-organic frameworks; BET theory; nitrogen isotherms; BET area; BET consistency criteria
Affiliations: Department of Chemistry, Faculty of Science, King Abdulaziz University, Jeddah 22254, Saudi Arabia

Abstract:  Metal-organic frameworks (MOFs) can exhibit exceptionally high surface areas, which are experimentally estimated by applying the BET theory to measured nitrogen isotherms. The Brunauer, Emmett, and Teller (BET)-estimated nitrogen monolayer loading is thus converted to a "BET area," but the meaning of MOF BET areas remains under debate. Recent emphasis has been placed on the usage of four so-called "BET consistency criteria." Using these criteria and simulated nitrogen isotherms for perfect crystals, we calculated BET areas for graphene and 25 MOFs having different pore-size distributions. BET areas were compared with their corresponding geometrically calculated, nitrogen-accessible surface areas (NASAs). Analysis of simulation snapshots elucidated the contributions of "pore-filling" and "monolayer-formation" to the nitrogen adsorption loadings in different MOF pores, revealing the origin of inaccuracies in BET-calculated monolayer loadings, which largely explain discrepancies between BET areas and NASAs. We also find that even if all consistency criteria are satisfied, the BET calculation can significantly overestimate the true monolayer loading, especially in MOFs combining mesopores (d ≥ 20 Å) and large micropores (d = 10-20 Å), due to the overlap of pore-filling and monolayer-formation regimes of these two kinds of pores. While it is not always possible to satisfy all consistency criteria, it is critical to minimize the deviation from these criteria during BET range selection to consistently compare BET areas of different MOFs and for comparing simulated and experimental BET areas of a given MOF. To accurately assess the quality of a MOF sample, it is best to compare experimental BET areas with simulated BET areas rather than with calculated NASAs. 

Retracted: No

PubPeer comments:
 Figure 1.  Scanning electron photomicrographs of (A) Pectin microspheres (original magnification x422) and (B) Eudragit-coated pectin microsphere (original magnification x3.06K). MS indicates microspheres. ![file] Fig 1 from [Bilthare Jain (2013)](http: www.ijpaonline.info index.php ijpaonline article view 29) - no DOI or PMID, so not indexed in PubPeer.  (B) SEM Photomicrograph of eudragit-S100 coated starch microspheres (650X) ![file] Are they pectin microspheres and Eudragit-coated **pectin** microspheres, or a single group of eudragit-coated **starch** microspheres? Perhaps the original 2007 authors or the 2013 authors can tell us. ,
Fungicidal synergistic effect of biogenically synthesized zinc oxide and copper oxide nanoparticles against Alternaria citri causing citrus black rot disease
Authors: Yamin Bibi
Momina Sardar
Waseem Ahmed
Sobia Nisa
Maimoona Sabir
Muhammad Mumtaz Khan
Waqas Ahmed
Abdul Qayyum
Samha Al Ayoubi
Journal: Saudi Journal of Biological Sciences (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Citrus black rot; Copper oxide nanoparticles; SEM; Scherrer equation; XRD
Affiliations: Department of Microbiology, The University of Haripur, Haripur 22620, Pakistan., Department of General Sciences, Prince Sultan University, Rafha Street, Riyadh, Saudi Arabia., Department of Botany, PMAS-Arid Agriculture University Rawalpindi, Rawalpindi 46300, Pakistan., Department of Horticulture, The University of Haripur, Haripur 22620, Pakistan., Department of Agronomy, The University of Haripur, Haripur 22620, Pakistan.

Abstract:  Citrus black rot disease being caused by Alternaria citri is a major disease of citrus plants with 30-35% economic loss annually. Fungicides had not been effective in the control of this disease during last few decades. In the present study, antifungal role of green synthesized zinc oxide (ZnO) and copper oxide (CuO) nanoparticles (NPs) were studied against Alternaria citri. Alternaria citri was isolated from disease fruits samples and was identified by staining with lacto phenol cotton blue. Furthermore, CuO and ZnO NPs were synthesized by utilizing the lemon peels extract as the reducing and capping agent. Nanoparticles were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM) techniques. From the XRD data, the calculated size of CuO NPs was to be 18 nm and ZnO NPs was16.8 nm using Scherrer equation. The SEM analyses revealed the surface morphology of all the metal oxide NPs synthesized were rounded, elongated and or spherical in the shape. The zone of inhibition was observed to be 50 ± 0.5 mm by CuO NPs, followed by 51.5 ± 0.5 mm by ZnO NPs and maximum zone of antifungal inhibition was observed to be 53 ± 0.6 mm by mix metal oxide NPs. The results of minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) of the synthesized nanoparticles showed that at the certain concentrations (80 mg ml-1), these NPs were capable of inhibiting the fungal growth, whereas above that specified concentrations (100 mg ml-1), NPs completely inhibited the fungal growth. Based on these findings, the green synthesized NPs can be used as alternative to fungicide in order to control the citrus black rot disease. 

Retracted: No

PubPeer comments:
 Figure 7, 9, and 11: There are duplicates within and between figures that should be unique, some are different photos, but show the same plate. I ve added the coloured boxes to show where I mean. Would the authors please comment? ![file] ,
Interplay between REST and nucleolin transcription factors: a key mechanism in the overexpression of genes upon increased phosphorylation
Authors: Rossen Donev
Baalasubramanian Sivasankar
Paul Brennan
B Paul Morgan
Martin Kolev
Teeo Tediose
Journal: Nucleic Acids Research (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: kinases; REST; nucleolin; phosphorylated; non-phosphorylated
Affiliations: Department of Infection, Immunity and Biochemistry, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.

Abstract:  Non-malignant cells can be transformed via the activation of kinases that control degradation of neural-restrictive silencer factor (REST). Here, we identify a mechanism that contributes to the activation of genes, expression of which is controlled by responsive elements containing overlapping binding sites for REST and nucleolin. We demonstrate that both phosphorylated and non-phosphorylated nucleolin-bound DNA; however, only phosphorylated nucleolin successfully competed with either full-length REST or a REST-derived DNA-binding peptide, REST68, for binding to the overlapping binding sites. We show that this interplay between the two transcription factors regulates the activation of cell survival and immunomodulatory genes in tumors and non-malignant cells with activated protein kinase C, which is accompanied with alterations in cell proliferation and apoptosis. We propose a model for the regulation of these genes, which brings a new insight into the molecular mechanisms that control cellular transformation driven by activation of protein kinases. 

Retracted: No

PubPeer comments:
 https: bylinetimes.com 2021 04 21 scientist-linked-to-great-barrington-declaration-embroiled-in-world-health-organization-conflict-of-interest In which we learn that the F1000 article has been rejected by its first referee. https: f1000research.com articles 10-232 v1#referee-response-82591 ,
Molecular engineering of a TBET-based two-photon fluorescent probe for ratiometric imaging of living cells and tissues
Authors: Liyi Zhou
Qianqian Wang
Aili Luo
Weihong Tan
Xiaobing Zhang
Yifan Lv
Yongxiang Wu
Jing Zhang
Yuan Wu
Guojiang Mao
Journal: Journal of the American Chemical Society (2014)
Discipline: CHEMISTRY
Keywords: two-photon microscopy; fluorescent imaging; biological events; living cells; tissues
Affiliations: Molecular Sciences and Biomedicine Laboratory, State Key Laboratory for Chemo/Biosensing and Chemometrics, College of Chemistry and Chemical Engineering, College of Biology, Collaborative Innovation Center for Molecular Engineering and Theranostics, Hunan University , Changsha, Hunan 410082, China., Molecular Sciences and Biomedicine
Laboratory, State Key Laboratory for Chemo/Biosensing and Chemometrics,
College of Chemistry and Chemical Engineering, College of Biology,
Collaborative Innovation Center for Molecular Engineering and Theranostics, Hunan University, Changsha, Hunan 410082, China

Abstract:  In contrast to one-photon microscopy, two-photon probe-based fluorescent imaging can provide improved three-dimensional spatial localization and increased imaging depth. Consequently, it has become one of the most attractive techniques for studying biological events in living cells and tissues. However, the quantitation of these probes is primarily based on single-emission intensity change, which tends to be affected by a variety of environmental factors. Ratiometric probes, on the other hand, can eliminate these interferences by the built-in correction of the dual emission bands, resulting in a more favorable system for imaging living cells and tissues. Herein, for the first time, we adopted a through-bond energy transfer (TBET) strategy to design and synthesize a small molecular ratiometric two-photon fluorescent probe for imaging living cells and tissues in real time. Specifically, a two-photon fluorophore (D-π-A-structured naphthalene derivative) and a rhodamine B fluorophore are directly connected by electronically conjugated bond to form a TBET probe, or Np-Rh, which shows a target-modulated ratiometric two-photon fluorescence response with highly efficient energy transfer (93.7%) and two well-resolved emission peaks separated by 100 nm. This novel probe was then applied for two-photon imaging of living cells and tissues and showed high ratiometric imaging resolution and deep-tissue imaging depth of 180 μm, thus demonstrating its practical application in biological systems. 

Retracted: No

PubPeer comments:
 Figure 3 ![file] ,
Differential effect of transforming growth factor beta (TGF-beta) on the genes encoding hyaluronan synthases and utilization of the p38 MAPK pathway in TGF-beta-induced hyaluronan synthase 1 activation
Authors: Christine Pollaschek
Karl M Stuhlmeier
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: hyaluronan; rheumatoid arthritis; genes; hyaluronan synthases; signaling pathways
Affiliations: Ludwig Boltzmann Institute for Rheumatology and Balneology, Kurbadstrasse 10, POB 78, A-1107 Vienna, Austria. 

Abstract:  Unfettered hyaluronan (HA) production is a hallmark of rheumatoid arthritis. The discovery of three genes encoding hyaluronan synthases (HASs) allows for the investigation of the signaling pathways leading to the activation of these genes. Our objective is to further understanding of the regulation of these genes as well as to find ways to prevent undesired gene activation. Human fibroblast-like synoviocytes were used in these experiments. mRNA levels of HAS were monitored by reverse transcriptase-PCR. A series of specific kinase inhibitors were used to investigate intracellular pathways leading to the up-regulation of HAS1. Our experiments, testing a series of stimuli including tumor necrosis factor alpha (TNFalpha), demonstrate that TGF-beta is the most potent stimulus for HAS1 transcription. TGF-beta activates HAS1 in a dose-dependent manner with a maximum effect at a concentration of 0.5-1 ng/ml. TGF-beta-induced HAS1 mRNA can be detected within 60 min and reaches maximal levels at 6 h. Furthermore, TGF-beta treatment leads to an increase in synthase activity as determined by HA ELISA and by in vitro HA synthase assays. In contrast to the activatory effect on HAS1, TGF-beta dose-dependently suppresses HAS3 mRNA. As to the mode of action of TGF-beta-induced HAS1 mRNA activation, our experiments reveal that blocking p38 MAPK inhibited the TGF-beta effect by 90%, blocking the MEK pathway led to an inhibition by 40%, and blocking the JNK pathway had no effect. The presented data might contribute to a better understanding of the role of TGF-beta and of HA in the pathology of diseases. 

Retracted: No

PubPeer comments:
 Figure 7A. * Pink boxes: The purple and orange lines appear to show very similar plots. * Blue boxes: The red and green lines appear to show very similar plots. ![file] , 
 Figure 7C. * Green boxes: Some parts of the top plot appear to be visible multiple times ![file] , 
 Correction, [20 May 2021] . --------------------- In the original published work, Figure 7a, 7c and Figure S11 are incorrect. The correct Figures are presented below ![] ![] Accordingly, the relevant paragraph on Page 9 should read as follows: u201cThe diffraction peaks located at about 33.0u00b0 and 35.4u00b0 can be indexed into (100) and (101) planes of Li2O2 (JCPDS Card No. 74-0115) and no other phases can be observed, unambiguously indicating the generated Li2O2 as the dominant oxygen reduction products for all the three discharged electrodes.[48,49]u201d The conclusions of the work are not affected by these errors. The authors apologize for any inconvenience caused. ,
Magnetically controlled release of cisplatin from superparamagnetic starch nanoparticles
Authors: Sweta Likhitkar
A K Bajpai
Journal: Carbohydrate Polymers (2012)
Discipline: CHEMISTRY
Keywords: Anticancer; Cisplatin; Drug delivery; Iron oxide; Nanoparticles

Abstract:  The present study involves a novel strategy for the preparation of superparamagnetic nanoparticles of crosslinked starch impregnated with homogeneously dispersed nanosized iron oxide. The nanoparticles were loaded with an anticancer drug 'cisplatin' and the drug release kinetics was investigated spectrophotometrically at physiological pH (7.4). The nanoparticles were characterized by Fourier transform infra red (FTIR) spectroscopy, transmission electron microscopy (TEM), X-ray diffraction and magnetization studies. The particle size of magnetic starch nanoparticles was found to lie in the range of 20-90nm. The influence of factors like chemical composition of nanoparticles, pH and temperature of the release media and applied magnetic field was investigated on the release profiles of the drug. The prepared nanoparticles could provide a possible pathway for targeted and controlled delivery of anticancer drugs minimizing side effects and achieving higher efficacy. 

Retracted: No

PubPeer comments:
  Fig. 3. ... (B) the TEM image of iron oxide impregnated starch nanoparticles contains repeated sections of substrate. ![file] Curiously, those sections are not present in a later presentation of the same image as Fig 4(b) of [Bajpai Likhitkar (2013)] , mislabelled as  crosslinked starch nanoparticles. Has this version been retouched? ![] , 
  Fig. 2. ... (B) X-ray diffraction pattern of u2013 (a) starch nanoparticles and (b) iron oxide impregnated starch nanoparticles. ![file] The figure is repeated as Fig 3 of [Baypai Likhitkar (2013)] and Fig 3 of [Likhitkar Baypai (2014)] , so I ll copy-paste my comment from those threads:  Remarkable resemblance between the patterns around the 2.theta = 15-20 deg peaks. ![] ,
Up-regulation of microRNA-574 attenuates lipopolysaccharide- or cecal ligation and puncture-induced sepsis associated with acute lung injury
Authors: Hong Li
Wenwen Sun
Jin Gu
Journal: Cell biochemistry and function (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: acute lung injury; endoplasmic reticulum stress; miR-574; sepsis.
Affiliations: Clinic and Research Center of Tuberculosis, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.

Abstract:  Acute lung injury (ALI) is the most vulnerable organ in sepsis, however, its underlying mechanism remains unclear. Cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry. The expressions of miR-574, Complement 3 (C3), glucose regulatory protein 78 (GRP78), C/EBP homologous protein (CHOP) and Caspase-12 were determined using quantitative real time (qRT)-PCR and Western blot. Histopathology of mice was stained by haematoxylin and eosin staining. The levels of tumour necrosis factor-α (TNF-α) and interleukin (IL)-1β were determined using ELISA. The expression of miR-574 was positively correlated with cell viability in lipopolysaccharide (LPS)-treated cells. Cell viability was improved and apoptosis was inhibited by mimics. Meanwhile, the levels of GRP78, CHOP and Caspase-12 were suppressed by mimics and agomir in LPS-treated human bronchial epithelial (HBE) cells and cecal ligation and puncture (CLP)-treated mice. In vivo, lung tissue damages were ameliorated by agomir, which also decreased the levels of neutrophils, macrophages and albumin. C3 was a target gene of miR-574 and could be decreased by mimics. SiC3 enhanced cell viability and inhibited apoptosis, however, it suppressed the mRNA levels of GRP78, CHOP and Caspase-12. Up-regulation of miR-574 attenuated sepsis-induced lung injury may be by promoting C3 down-regulation and reducing sepsis-induced endoplasmic reticulum stress (ERS). SIGNIFICANCE OF THE STUDY: Clinically, the mortality rate of ALI induced by sepsis remains at a high level, thus, clarifying the mechanism of induction of ALI through pathogen infection will provide a new target for clinical treatment of ALI. In this study, up-regulation of miR-574 attenuated sepsis-induced lung injury may be by promoting C3 down-regulation and reducing sepsis-induced ERS. Our study provides a deeper understanding of sepsis. 

Retracted: No

PubPeer comments:
 I m pretty sure this is a formatting mistake, but figures 6 7 are the same in both the HTML and PDF of this paper (legends are different) ,
Bcl-2 Phosphorylation by p38 MAPK: identification of target sites and biologic consequences
Authors: Paolo Bonini
Giovanna De Chiara
Maria Elena Marcocci
Anna Teresa Palamara
Enrico Garaci
Maria Lucibello
Sarah Amodei
Maria Torcia
Yukiro Higashimoto
Gianluca Damonte
Federico Cozzolino
Paolo Rosini
Tommaso Russo
Andrea Armirotti
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bcl-2; phosphorylation; p38 MAPK; apoptosis; serine
Affiliations: Department of Cell Biology and Neuroscience, Istituto Superiore di Sanità, Rome, Italy. 

Abstract:  The antiapoptotic role of Bcl-2 can be regulated by its phosphorylation in serine and threonine residues located in a nonstructured loop that links BH3 and BH4 domains. p38 MAPK has been identified as one of the kinases able to mediate such phosphorylation, through direct interaction with Bcl-2 protein in the mitochondrial compartment. In this study, we identify, by using mass spectrometry techniques and specific anti-phosphopeptide antibodies, Ser(87) and Thr(56) as the Bcl-2 residues phosphorylated by p38 MAPK and show that phosphorylation of these residues is always associated with a decrease in the antiapoptotic potential of Bcl-2 protein. Furthermore, we obtained evidence that p38 MAPK-induced Bcl-2 phosphorylation plays a key role in the early events following serum deprivation in embryonic fibroblasts. Both cytochrome c release and caspase activation triggered by p38 MAPK activation and Bcl-2 phosphorylation are absent in embryonic fibroblasts from p38alpha knock-out mice (p38alpha(-/-) MEF), whereas they occur within 12 h of serum withdrawal in p38alpha(+/+) MEF; moreover, they can be prevented by p38 MAPK inhibitors and are not associated with the synthesis of the proapoptotic proteins Bax and Fas. Thus, Bcl-2 phosphorylation by activated p38 MAPK is a key event in the early induction of apoptosis under conditions of cellular stress. 

Retracted: No

PubPeer comments:
null, 
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 ![file] So many similar bands in the immunoblot of Figure 6, shown in colored boxes. Especially in the p38a+ +MEF panel, the bands in the middle (blue boxes) of the 16hr negative group and the 24hr negative group share much more similar than expected. Could the authors explain why? ,
Effects of Artesunate on chondrocyte proliferation, apoptosis and autophagy through the PI3K/AKT/mTOR signaling pathway in rat models with rheumatoid arthritis
Authors: Hai-Yan Qiu
Fa-Bo Feng
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; Artesunate; Autophagy; Chondrocyte; PI3K/AKT/mTOR signaling pathway
Affiliations: Department of Orthopedics, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, PR China., Department of Endocrinology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou 310006, PR China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Concern was raised about the reliability of the Western blot results in Figure 5D and 5F, which appear to have a similar phenotype as contained within another publication, as detailed here: https://pubpeer.com/publications/CD4DF7B6DCA28182EC6809846F3653; and here: https://docs.google.com/spreadsheets/d/1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY/edit#gid=262337249. Concerns were also raised about the provenance of the flow cytometry data in Figure 7A. In addition, suspected duplications were detected in Western blots contained within Figure 5E and 5F. The journal requested the corresponding author comment on these concerns and provide raw data. The corresponding author communicated that the raw data was not available and some of the results were not repeatable and therefore not solid enough to support the conclusions. The authors requested retraction of this article. The Editor-in-Chief assessed this case and decided to retract the article. 

Retracted: No

PubPeer comments:
 I am concerned that there appears to be at least four examples of overlap between images that represent different conditions. ![file] ,