PReD-Bench/PRed-Bench huggingface dataset:
miR-143-3p impacts on pulmonary inflammatory factors and cell apoptosis in mice with mycoplasmal pneumonia by regulating TLR4/MyD88/NF-κB pathway
Authors: Donghai Liu
Yongjun Wang
Yan Xu
Shuying Wang
Yongsheng Shi
Huan Li
Hanyi Li
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TLR4/MyD88/NF-κB signaling pathway; apoptosis; inflammation; miR-143-3p; mycoplasmal pneumonia.
Affiliations: Department of Pediatric Respiratory Medicine, Gansu Provincial Maternity and Child-Care Hospital, Lanzhou, Gansu Province, China, Department of Rehabilitation, Gansu Province Hospital Rehabilitation Center, Lanzhou, Gansu Province, China

Abstract:  miR-143-3p is correlated with inflammatory pain responses, such as hsa-miR-143-3p expression reduction in fibromyalgia. The present study aimed to explore the effects of miR-143-3p and Toll-like receptor (TLR) 4/myeloid differentiation factor 88 (MyD88)/NF-κB signaling pathway on pulmonary inflammatory factors levels and alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice. Twenty mice were selected as normal group. The 120 successfully modeled Mycoplasma pneumoniae (MP) infection mice were randomly divided into model group (without any treatment), negative control (NC) group (injected with NC mimic), miR-143-3p mimic group (injected with miR-143-3p mimic), miR-143-3p inhibitor group (injected with miR-143-3p inhibitor), TAK-242 group (treatment with TAK-242), and miR-143-3p inhibitor + TAK-242 group (treatment with miR-143-3p inhibitor + TAK-242). Compared with model group, model mice had up-regulated miR-143-3p expression and decreased MyD88 and p-NF-κB p50 protein expressions (all P&lt;0.05); Model mice treated with miR-143-3p mimic and TAK-242 had reduced interleukin (IL)-2 and tumor necrosis factor (TNF)-α contents and protein expressions of MyD88, p-NF-κB p50, increased IL-10 content, fewer alveolar epithelial cell apoptosis, lower Bax expression and higher Bcl-2 expression (all P&lt;0.05); however, mice with miR-143-3p inhibitor treatment showed opposite trends in terms of above indicators. The exacerbation of mycoplasmal pneumonia caused by miR-143-3p inhibitor was partly improved by miR-143-3p inhibitor + TAK-242 combination treatment (all P&lt;0.05). Therefore, up-regulation of miR-143-3p expression may ameliorate pulmonary inflammatory factors levels and reduce alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice by inhibiting TLR4/MyD88/NF-κB signaling pathway. 

Retracted: No

PubPeer comments:
 The western blot images in figure 5C appear atypical with no background. Could the authors please provide the uncropped original scan? *** ![file] , 
 March 31, 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Association of atopic dermatitis with depression, anxiety, and suicidal ideation in children and adults: A systematic review and meta-analysis
Authors: Anne-Sofie Halling-Overgaard
Lone Skov
Amalie Thorsti Møller Rønnstad
Alexander Egeberg
Jacob P Thyssen
Carsten R Hamann
Journal: Journal of the American Academy of Dermatology (2018)
Discipline: CLINICAL MEDICINE
Keywords: anxiety; atopic dermatitis; depression; meta-analysis; suicidal ideation
Affiliations: Department of Dermatology and Allergy, Herlev and Gentofte Hospital, Hellerup, Denmark; Copenhagen Research Group for Inflammatory Skin, Herlev and Gentofte Hospital, Hellerup, Denmark., Department of Dermatology and Allergy, Herlev and Gentofte Hospital, Hellerup, Denmark; Copenhagen Research Group for Inflammatory Skin, Herlev and Gentofte Hospital, Hellerup, Denmark; National Allergy Research Centre, Herlev and Gentofte Hospital, Hellerup, Denmark. Electronic address: .

Abstract:  Background: Atopic dermatitis (AD) has been associated with anxiety and depression, but the magnitude of the alleged association is unknown. Objective: To perform a systematic review and meta-analysis of the association between AD in children and adults and, respectively, depression, anxiety, and suicidal behavior. Methods: The medical databases PubMed, Embase, and PsychINFO were searched. Results: There was a significant association between adult AD and, respectively, depression (pooled odds ratio [OR], 2.19; 95% confidence interval [CI], 1.87-2.57) and anxiety (pooled OR, 2.19; 95% CI, 1.75-2.73). AD was also associated with depression in children (pooled OR, 1.27; 95% CI, 1.12-1.45); few data were available for anxiety. A positive association was found between AD in adults and adolescents and suicidal ideation (pooled OR, 4.32; 95% CI, 1.93-9.66). Only a few studies examined the risk of completed suicide, but the majority showed a positive association between completed suicide and AD. Limitations: Included studies used different definitions of depression and anxiety, and few studies examined the severity of AD. Conclusion: Depression, anxiety, and suicidal ideation should be considered by doctors when treating patients with AD. Because AD disease improvement appears to reduce these risks, this should be a priority. 

Retracted: No

PubPeer comments:
 There is a minor error in name of author: forest plot says Bahreinia but it should be Bahreinian 2011 ,
From neurons to microglia, with complements
Authors: Jonathan Kipnis
Noël C Derecki
Journal: Nature Neuroscience (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: astrocytic; transforming growth factor-β; complement-mediated removal; weak synapses; microglia
Affiliations: Center for Brain Immunology and Glia, Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.

Abstract: A study in this issue of Nature Neuroscience demonstrates that astrocytic transforming growth factor-β facilitates complement-mediated removal of weak synapses by microglia during the synaptic pruning period.

Retracted: Yes

PubPeer comments:
 Retraction of: Nature Neuroscience https: www.nature.com articles nn.3579, published online 22 November 2013. In view of the fact that the article u2018TGF-u03b2 signaling regulates neuronal C1q expression and developmental synaptic refinementu2019, by Allison R. Bialas and Beth Stevens, has been retracted by the authors , we retract this News Views highlighting the study, because it relied on the validity of the data presented therein. https: www.nature.com articles s41593-021-00892-8 ,
Cyanidin-3-O-β-glucoside inactivates NLRP3 inflammasome and alleviates alcoholic steatohepatitis via SirT1/NF-κB signaling pathway
Authors: Lili Yang
Yingying Gu
Yuanling Huang
Ting Wan
Xuye Jiang
Nengzhi Pang
Sufan Wang
Zhenfeng Zhang
Yujia Zhou
Jing Luo
Journal: Free Radical Biology and Medicine (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Alcoholic steatohepatitis (ASH); Cyanidin-3-O-β-glucoside (Cy-3-G); NLRP3 inflammasome; Oxidative stress; SirT1.
Affiliations: Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong, China., Department of Nutrition, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China., Department of Nutrition, Huizhou First People's Hospital, Huizhou Guangdong Province, 516003, China., Department of Nutrition, Binhaiwan Central Hospital of Dongguan, The Dongguan Affiliated Hospital of Medical College of Jinan University, Dongguan, Guangdong, China.

Abstract:  Alcoholic liver disease (ALD) is a major cause of liver disease worldwide. In patients with ALD, an increased level of hepatic inflammasome components was observed, together with an increased circulating pro-inflammatory cytokines. Cyanidin-3-O-β-glucoside (Cy-3-G) is a bioactive compound belonging to the anthocyanin group, which widely exists in deep-colored fruits and vegetables. Consumption of Cy-3-G is associated with lower risks of non-alcoholic fatty liver disease (NAFLD), liver fibrosis, obesity, atherosclerosis, and inflammation. However, whether Cy-3-G has effects on inflammasome formation and activation thereby protects against alcohol-induced liver damage remain elusive. In this study, we identified that dietary provision of Cy-3-G remarkably attenuated liver damage caused by excess energy intake and alcohol consumption. Supplement with Cy-3-G mediated NAD+ homeostasis, which stimulated SirT1 activity, resulting in suppressed NF-κB acetylation. Interestingly, Cy-3-G treatment suppressed NF-κB acetylation when SirT1 action was blunted by selective antagonist, and subsequently suppressed NLRP3 inflammasome activation and proinflammatory cytokines release in hepatic cell lines. Our findings first demonstrate that Cy-3-G at a physiologically achievable dosage alleviates alcohol-induced hepatic inflammation via inactivation of NLRP3 inflammasome and deacetylation of NF-κB, suggesting a promising therapeutic approach to alleviate alcohol-induced liver damage. 

Retracted: No

PubPeer comments:
 Major: Figures 3A and 5A, the beta-actin loading controls look very similar. Arguably, the experimental conditions were the same between the two panels but based on the shape of Western blot bands in Figure 5A, Nuc-NF-kB, Lamin A, Cyto-NF-kB, and Sirt1 were not ran in the same gel as beta-actin. This may have implications for the protein amount quantifications. Minor: Panel IDs in Figure 5 do not seem to match the Panel IDs in the legend to Figure 5. ,
Casein‐enhanced uptake and disease‐modifying bioactivity of ingested extracellular vesicles
Authors: Mario Fournier
K Candis Jones-Ungerleider
Eduardo Marbán
Mark A Aminzadeh
Akbarshakh Akhmerov
Jackelyn B Valle
Journal: Journal of Extracellular Vesicles (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: casein; extracellular vesicles; ingestion.
Affiliations: Cedars-Sinai Medical Center Smidt Heart Institute Los Angeles California USA.

Abstract:  Extracellular vesicles (EVs) from cardiac stromal cells, developed as therapeutic candidates, improve dystrophic muscle function when administered parenterally, but oral delivery remains untested. We find that casein, the dominant protein in breast milk, enhances the uptake and bioactivity of ingested heart-derived EVs, altering gene expression in blood cells and enhancing muscle function in mdx mice with muscular dystrophy. Thus, EVs, administered orally, are absorbed and exert disease-modifying bioactivity in vivo. Formulating EVs with casein enhances uptake and markedly expands the range of potential therapeutic applications. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
 #1 Figure 5. Much more similar than expected. ![file] ,
New role for granulocyte colony-stimulating factor-induced extracellular signal-regulated kinase 1/2 in histone modification and retinoic acid receptor α recruitment to gene promoters: relevance to acute promyelocytic leukemia cell differentiation
Authors: G Beinse
B Cassinat
P Fenaux
O Chourbagi
C Ferry
C Rochette Egly
G Despouy
F Zassadowski
L Llopis
V Duong
A Cras
N Bruck
E Lainey
C Chomienne
Journal: Molecular and Cellular Biology (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: granulocytic differentiation; all-trans retinoic acid; acute promyelocytic leukemia; synergism; granulocyte colony-stimulating factor
Affiliations: INSERM UMR-S-940, Université Paris Diderot, Hopital Saint-Louis, 75010 Paris, France. 

Abstract:  The induction of the granulocytic differentiation of leukemic cells by all-trans retinoic acid (RA) has been a major breakthrough in terms of survival for acute promyelocytic leukemia (APL) patients. Here we highlight the synergism and the underlying novel mechanism between RA and the granulocyte colony-stimulating factor (G-CSF) to restore differentiation of RA-refractory APL blasts. First, we show that in RA-refractory APL cells (UF-1 cell line), PML-RA receptor alpha (RARα) is not released from target promoters in response to RA, resulting in the maintenance of chromatin repression. Consequently, RARα cannot be recruited, and the RA target genes are not activated. We then deciphered how the combination of G-CSF and RA successfully restored the activation of RA target genes to levels achieved in RA-sensitive APL cells. We demonstrate that G-CSF restores RARα recruitment to target gene promoters through the activation of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway and the subsequent derepression of chromatin. Thus, combinatorial activation of cytokines and RARs potentiates transcriptional activity through epigenetic modifications induced by specific signaling pathways. 

Retracted: No

PubPeer comments:
 2017 correction. http: mcb.asm.org content 37 14 e00222-17.short , 
 The correction reads:  *Fig 1Bc: An error was made during assembly of the figure that resulted in inadvertent image duplication. The corrected image should appear as shown below. The conclusions are unchanged by this correction, but we apologize for any confusion this error might have caused.* Here is the original Figure 1B, marked with blue boxes that highlight the duplicated panels, as reported to the journal in September 2016. ![file] I thank the authors and journal staff for addressing this error. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Bub1 and CENP-F can contribute to Kaposi's sarcoma-associated herpesvirus genome persistence by targeting LANA to kinetochores
Authors: Subhash C Verma
Bingyi Xiao
Jie Lu
Erle S Robertson
Rajeev Kaul
Qiliang Cai
Abhik Saha
Journal: Journal of virology (2010)
Discipline: MICROBIOLOGY
Keywords: LANA; KSHV; CENP-F; Bub1; genome tethering
Affiliations: Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA., Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Abstract:  The latency-associated nuclear antigen (LANA) encoded by Kaposi's sarcoma-associated herpesvirus (KSHV) is critical for segregation of viral episomes to progeny nuclei and allows for maintenance of the viral genome in newly divided daughter cells. LANA binds to KSHV terminal repeat (TR) DNA and simultaneously associates with chromatin-bound cellular proteins. This process tethers the viral episomes to host chromosomes. However, the mechanism of tethering is complex and involves multiple protein-protein interactions. Our previous proteomics studies which showed the association of LANA with centromeric protein F (CENP-F) prompted us to further study whether LANA targets centromeric proteins for persistence of KSHV episomes during cell division. Here we show that LANA colocalized with CENP-F as speckles, some of which are paired at centromeric regions of a subset of chromosomes in KSHV-infected JSC-1 cells. We also confirm that both the amino and carboxy termini of LANA can bind to CENP-F. Moreover, LANA associated with another kinetochore protein, Bub1 (budding uninhibited by benzimidazole 1), which is known to form a complex with CENP-F. Importantly, we demonstrated the dynamic association of LANA and Bub1/CENP-F and the colocalization between Bub1, LANA, and the KSHV episome tethered to the host chromosome using fluorescence in situ hybridization (FISH). Knockdown of Bub1 expression by lentivirus-delivered short hairpin RNA (shRNA) dramatically reduced the number of KSHV genome copies, whereas no dramatic effect was seen with CENP-F knockdown. Therefore, the interaction between LANA and the kinetochore proteins CENP-F and Bub1 is important for KSHV genome tethering and its segregation to new daughter cells, with Bub1 potentially playing a more critical role in the long-term persistence of the viral genome in the infected cell. 

Retracted: No

PubPeer comments:
 Figure 2F. Much more similar than you would expect. https: imgur.com BblsEkY , 
 Last author appears to be on this journalu2019s editorial board: https: jvi.asm.org content board-editors ,
Chitosan-Chondroitin sulfate based polyelectrolyte complex for effective management of chronic wounds
Authors: Swati Sharma
K Laxmi Swetha
Aniruddha Roy
Journal: International Journal of Biological Macromolecules (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Chitosan; Chondroitin sulfate; In-situ scaffold; Polyelectrolyte complex; Wound healing.
Affiliations: Department of Pharmacy, Birla Institute of Technology & Science, Pilani, Vidya Vihar, Pilani, Rajasthan 333031, India., Department of Pharmacy, Birla Institute of Technology & Science, Pilani, Vidya Vihar, Pilani, Rajasthan 333031, India. Electronic address: .

Abstract:  Acute and chronic wound remain an unresolved clinical problem among various demographic groups. Traditional marketed products focus mainly on inhibition of bacterial growth at the wound site neglecting the tissue repair, which significantly affect the healing rate. It would be highly beneficial if a wound healing material can be developed which has both antibacterial as well as tissue regenerating potential. We have prepared a polyelectrolyte complex (PEC) using chitosan (CH) and chondroitin sulfate (CS) which can form an in-situ scaffold by spontaneous mixing. The fabrication of CH-CS PEC was optimized using Quality-By-Design (QbD) approach. The prepared PEC showed very high swelling and porosity property. It was found to be non-hemolytic with good blood compatibility and low blood clotting index. It also exhibited good antibacterial activity against both gram-positive and gram-negative bacteria. The cell proliferation study exhibited good cytocompatibility and almost four-fold increase in cell density when treated with CH-CS PEC compared to control. In summary, we demonstrated that the prepared CH-CS PEC showed good blood compatibility, high antibacterial effect, and promoted wound healing potentially by stimulating fibroblast growth, making it an ideal wound dressing material. 

Retracted: No

PubPeer comments:
 ![file] Figure 6 (A) : Fluorescent microscopic image of the cells marked in red are same only the exposure is changed. Although the are labeled to be of different groups. ,
MiRNA-146b-5p inhibits the malignant progression of gastric cancer by targeting TRAF6
Authors: Y-F Zang
J-N Ding
Y-L Ding
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MicroRNAs; miRNA-146b-5p; gastric cancer; GC; lymphatic metastasis
Affiliations: Department of Medicine, Queen Mary School, Medical College of Nanchang University, Nanchang, China. .

Abstract:  Objective: MicroRNAs (miRNAs) are 22 nucleotides long that are extensively expressed in eukaryotes. They are vital regulators in pathological processes. This study aims to illustrate the role of miRNA-146b-5p in the development of gastric cancer (GC). Patients and methods: MiRNA-146b-5p levels in 62 GC species and matched paracancerous ones were detected. Influences of miRNA-146b-5p level on clinical parameters of GC patients were assessed. Phenotype changes of AGS and SGC-7901 cells overexpressing miRNA-146b-5p were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. Luciferase assay and rescue experiments were conducted to uncover the mechanism of miRNA-146b-5p in regulating the development of GC. Results: MiRNA-146b-5p was downregulated in GC species than paracancerous ones. Lower level of miRNA-146b-5p was observed in GC patients combined lymphatic metastasis and distant metastasis than those without metastases. In vitro overexpression of miRNA-146b-5p attenuated proliferative and migratory potentials of GC cells. TRAF6 was the target of miRNA-146b-5p, which was responsible for the development of GC regulated by miRNA-146b-5p. Conclusions: MiRNA-146b-5p level is negatively correlated to lymphatic metastasis and distant metastasis rates of GC. It suppresses the malignant development of GC by targeting TRAF6. 

Retracted: Yes

PubPeer comments:
 *[below]* Fig 3A from [Ding, Zang Ding (2020)] .  Protein ... levels of TRAF6 in AGS and SGC-7901 cells transfected with NC mimics and miRNA-146b-5p mimics . *[above]* Fig 3A from [Bao et al (2020)] .  Protein (A) ... of JAG1 in G401 cells transfected with NC mimics or miRNA-203a-5p mimics, and SK-NEP-1 cells transfected with NC inhibitor or miRNA-203a-5p inhibitor . ![file] Perhaps one or other team of authors could comment on the appearance of the same GAPDH loading controls in these wildly different contexts. , 
 Retracted [April 2021] .  The article u201cMiRNA-146b-5p inhibits the malignant progression of gastric cancer by targeting TRAF6, by J.-N. Ding, Y.-F. Zang, Y.-L. Ding, published in Eur Rev Med Pharmacol Sci 2020; 24 (17): 8837-8844u2013DOI: 10.26355 eurrev_202009_22823u2013PMID: 32964972u201d has been withdrawn from the authors due to some technical reasons (some data are not reproducible).  The Publisher apologizes for any inconvenience this may cause. ,
Influence of norcantharidin on proliferation, proliferation-related gene proteins proliferating cell nuclear antigen and Ki-67 of human gallbladder carcinoma GBC-SD cells
Authors: Jin-Ye Fu
Ze-Ming Zhao
Cun-Qiu Chen
Yue-Zu Fan
Journal: Hepatobiliary & Pancreatic Diseases International (2004)
Discipline: CLINICAL MEDICINE
Keywords: Gallbladder carcinoma; Norcantharidin; Proliferation; PCNA; Ki-67
Affiliations: Department of Surgery, Tongji Hospital of Tongji University, 389 Xincun Road, Shanghai 200065, China. 

Abstract:  Background: Gallbladder carcinoma is a highly lethal and aggressive disease with early metastasis, strong invasion and poor prognosis. Most patients with this disease are at the advanced and un-resectable stage and should be considered for palliative treatment such as chemotherapy and radiotherapy. Unfortunately, reports of chemotherapy and radiotherapy for gallbladder carcinoma are disappointing. We investigated the influence of norcantharidin (NCTD) on proliferation, proliferation-related gene proteins PCNA and Ki-67 of human gallbladder carcinoma GBC-SD cells in vitro. Methods: GBC-SD cell lines of human gallbladder carcinoma were cultured by the cell culture technique. The experiment was divided into NCTD group and control group. The tetrazolium-based colorimetric assay was used to evaluate cell growth. The streptavidin-biotin complex method was used to determine the expressions of proliferation-related gene proteins PCNA and Ki-67 of human gallbladder carcinoma GBC-SD cells. Results: NCTD inhibited the growth and proliferation of GBC-SD cells from 10 mg/L or after 6 hours in a dose-and time-dependent manner, with the IC50 value of 56.18 microg/ml at 48 hours. After treatment with NCTD, the expression of PCNA (0.932+/-0.031 vs. 0.318+/-0.023, P&lt;0.001) and Ki-67 (0.964+/-0.092 vs. 0.297+/-0.018, P&lt;0.001) proteins were decreased significantly. Conclusion: NCTD inhibits the proliferation of human gallbladder carcinoma GBC-SD cells in vitro and the expression of their proliferation-related gene proteins PCNA and Ki-67. 

Retracted: No

PubPeer comments:
 Figures 2 and 3. * Red boxes: Figure 2B (PCNA staining) appears to match Figure 3B (Ki-67 staining), albeit at a different zoom factor and rotated 180 degrees. ![file] ,
Novel thermal-sensitive hydrogel enhances both humoral and cell-mediated immune responses by intranasal vaccine delivery
Authors: Youbin Wu
Shipo Wu
Guanghui Ma
Meng Zhou
Lihua Hou
Wei Chen
Jie Wu
Zhiguo Su
Wei Wei
Journal: European Journal of Pharmaceutics and Biopharmaceutics (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Thermal sensitive hydrogel; HTCC; α, β-glycerophosphate; intranasal vaccine delivery; adenovirus
Affiliations: National Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, PR China.

Abstract:  A novel thermal sensitive hydrogel was formulated with N-[(2-hydroxy-3-trimethylammonium) propyl] chitosan chloride (HTCC) and α, β-glycerophosphate (α, β-GP). A serial of hydrogels containing different amount of GP and HTCC with diverse quarternize degree (QD, 41%, 59%, 79.5%, and 99%) were prepared and characterized by rheological method. The hydrogel was subsequently evaluated for intranasal vaccine delivery with adenovirus based Zaire Ebola virus glycoprotein antigen (Ad-GPZ). Results showed that moderate quarternized HTCC (60% and 79.5%) hydrogel/antigen formulations induced highest IgG, IgG1, and IgG2a antibody titers in serum, as well as mucosal IgA responses in lung wash, which may attributed to the prolonged antigen residence time due to the thermal-sensitivity of this hydrogel. Furthermore, CD8(+) splenocytes for IFN-γ positive cell assay and the release profile of Th1/Th2 type cytokines (IFN-γ, IL-2, IL-10, and IL-4) showed that hydrogel/Ad-GPZ generated an overwhelmingly enhanced Th1 biased cellular immune response. In addition, this hydrogel displayed low toxicity to nasal tissue and epithelial cells even by frequently intranasal dosing of hydrogel. All these results strongly supported this hydrogel as a safe and effective delivery system for nasal immunization. 

Retracted: No

PubPeer comments:
 Fig 6. ![file] I have concerns. ![file] ![file] , 
 Fig 5(a-g).  Fluorescence intensity detected after intranasal administration of NHS-Cy5 labeled Ad-GPZ in PBS or hydrogel at different time intervals. Did a mouse fall into the photocopier? ![file] ,
Shotgun proteomic analysis of ESBL-producing and non-ESBL-producing Klebsiella Pneumoniae clinical isolates
Authors: Samira Zakeer
Shymaa Enany
Ahmed A Sayed
Sameh Magdeldin
Journal: Microbiological Research (2020)
Discipline: MICROBIOLOGY
Keywords: ESBLs; Klebsiella pneumoniae; Proteomics.
Affiliations: Department of Microbiology and Immunology, Faculty of Pharmacy, Suez Canal University, Egypt. Electronic address: ., Department of Microbiology and Immunology, Faculty of Pharmacy, Suez Canal University, Egypt., Genomic Research Program, Basic Research Department, Children's Cancer Hospital Egypt 57357, 11441 Cairo, Egypt; Department of Biochemistry, Faculty of Science, Ain Shams University, Cairo, Egypt., Proteomics and Metabolomics Unit, Department of Basic Research, Children's Cancer Hospital Egypt 57357, 11441 Cairo, Egypt; Department of Physiology, Faculty of Veterinary Medicine, Suez Canal University, 41522 Ismailia, Egypt.

Abstract:  Klebsiella pneumoniae is a pathogenic bacterium that is responsible for a wide range of infections in humans. An increased rate of infections caused by multi-drug-resistant K. pneumoniae has been noted in the last two decades. The association between antimicrobial resistance and virulence is an important topic of study. Genomic tools have been used widely for the detection of virulence. In our study, we used proteomic analysis with mass spectrometry and bioinformatics tools to explore the virulence factors of both ESBL-producing and non-ESBL-producing K. pneumoniae and to determine the association between virulence and antimicrobial resistance in these clinical isolates. We have revealed different proteomic profiles and different pathways between the ESBL- and non-ESBL-producing groups. Many proteins involved in stress responses have been reported in the shared proteome between ESBL-and non-ESBL producers, such as ElaB protein, Lon protease, and universal stress proteins G and A. The virulence and pathogenicity of ESBL-producing bacteria were stronger than those of the non-ESBL-producing bacteria. Several unique virulence determinants were identified in ESBL-producing K. pneumoniae, such as proteins with lyase, catalase, isochorismatase, and oxidoreductase activity. 

Retracted: No

PubPeer comments:
 They quote: The proteins identified in this study are available in the PRIDE database (www.ebi.ac.uk pride) via ProteomeXchange with identifier PXD011693. But this code does not exist. , 
 #1 The data available here: https: www.ebi.ac.uk pride archive projects PXD011693 Please check the above mentioned link ,
Alternative ESC and ESC-Like Subunits of a Polycomb Group Histone Methyltransferase Complex Are Differentially Deployed during Drosophila Development
Authors: Richard S Jones
Ellen L Miller
Erica F Andersen
Liangjun Wang
Marcus L Vargas
Junyu Zhang
Judith Benes
Jeffrey A Simon
Neal Jahren
Journal: Molecular and Cellular Biology (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ESC; Polycomb group repressor; ESCL; E(Z); histone methyltransferase complex
Affiliations: Department of Biological Sciences, Southern Methodist University, Dallas, Texas 75275, USA., Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, Department of Biological Sciences, Southern Methodist University, Dallas, Texas 75275

Abstract:  The Extra sex combs (ESC) protein is a Polycomb group (PcG) repressor that is a key noncatalytic subunit in the ESC-Enhancer of zeste [E(Z)] histone methyltransferase complex. Survival of esc homozygotes to adulthood based solely on maternal product and peak ESC expression during embryonic stages indicate that ESC is most critical during early development. In contrast, two other PcG repressors in the same complex, E(Z) and Suppressor of zeste-12 [SU(Z)12], are required throughout development for viability and Hox gene repression. Here we describe a novel fly PcG repressor, called ESC-Like (ESCL), whose biochemical, molecular, and genetic properties can explain the long-standing paradox of ESC dispensability during postembryonic times. Developmental Western blots show that ESCL, which is 60% identical to ESC, is expressed with peak abundance during postembryonic stages. Recombinant complexes containing ESCL in place of ESC can methylate histone H3 with activity levels, and lysine specificity for K27, similar to that of the ESC-containing complex. Coimmunoprecipitations show that ESCL associates with E(Z) in postembryonic cells and chromatin immunoprecipitations show that ESCL tracks closely with E(Z) on Ubx regulatory DNA in wing discs. Furthermore, reduced escl+ dosage enhances esc loss-of-function phenotypes and double RNA interference knockdown of ESC/ESCL in wing disc-derived cells causes Ubx derepression. These results suggest that ESCL and ESC have similar functions in E(Z) methyltransferase complexes but are differentially deployed as development proceeds. 

Retracted: No

PubPeer comments:
 Figure 5. * Red boxes: The Gen panel in Figure 5B appears to overlap with that in Figure 5C. ![file] ,
SNS-314, a pan-Aurora kinase inhibitor, shows potent anti-tumor activity and dosing flexibility in vivo
Authors: Brian J Belmont
Michael J Romanowski
Marc J Evanchik
W Michael Flanagan
Pietro Taverna
Sean C Ritchie
Juli N Teague
Shannon O Harris
Ahmad Hashash
Anthony R Howlett
Jennifer P Arbitrario
Ute Hoch
Jeffrey W Jacobs
Stig K Hansen
Raymond V Fucini
Kristin M Zimmerman
Jeffrey A Silverman
Joni W Lam
David E Stockett
Jennifer N Hogan
Journal: Cancer Chemotherapy and Pharmacology (2010)
Discipline: CLINICAL MEDICINE
Keywords: Aurora kinases; SNS-314; inhibitor; cancer; tumor
Affiliations: Department of Pharmacology, Sunesis Pharmaceuticals, Inc., 395 Oyster Point Blvd., South S. Francisco, CA 94080, USA.

Abstract:  Purpose: The Aurora family of serine/threonine kinases (Aurora-A, Aurora-B, and Aurora-C) plays a key role in cells orderly progression through mitosis. Elevated expression levels of Aurora kinases have been detected in a high percentage of melanoma, colon, breast, ovarian, gastric, and pancreatic tumors. We characterized the biological and pharmacological properties of SNS-314, an ATP-competitive, selective, and potent inhibitor of Aurora kinases. Methods: We studied the biochemical potency and selectivity of SNS-314 to inhibit Aurora kinases A, B, and C. The inhibition of cellular proliferation induced by SNS-314 was evaluated in a broad range of tumor cell lines and correlated to inhibition of histone H3 phosphorylation, inhibition of cell-cycle progression, increase in nuclear content and cell size, loss of viability, and induction of apoptosis. The dose and administration schedule of SNS-314 was optimized for in vivo efficacy in mouse xenograft models of human cancer. Results: In the HCT116 human colon cancer xenograft model, administration of 50 and 100 mg/kg SNS-314 led to dose-dependent inhibition of histone H3 phosphorylation for at least 10 h, indicating effective Aurora-B inhibition in vivo. HCT116 tumors from animals treated with SNS-314 showed potent and sustained responses including reduction of phosphorylated histone H3 levels, increased caspase-3 and appearance of increased nuclear size. The compound showed significant tumor growth inhibition in a dose-dependent manner under a variety of dosing schedules including weekly, bi-weekly, and 5 days on/9 days off. Conclusions: SNS-314 is a potent small-molecule inhibitor of Aurora kinases developed as a novel anti-cancer therapeutic agent for the treatment of diverse human malignancies. 

Retracted: No

PubPeer comments:
 Figure 5A. * Red ellipses: The left 2 or 3 p-HH3 lanes at 3h look similar to those at 10h. Reported to the journal together with 28 other papers in the summer of 2015, with a friendly reminder in April 2017, but no answer. With the exception of one paper, not a single one of those papers have been corrected or retracted. Could the authors please let me know if the journal ever contact them in the past five and a half years? ![file] ,
NF-kappaB activation by Helicobacter pylori requires Akt-mediated phosphorylation of p65
Authors: Masachika Senba
Jiro Fujita
Chihiro Sasakawa
Hirochika Kawakami
Koh Tomimori
Eriko Takeshima
Fukunori Kinjo
Hitomi Mimuro
Shigeki Sawada
Naoki Mori
Chie Ishikawa
Mariko Tomita
Journal: BMC microbiology (2009)
Discipline: MICROBIOLOGY
Keywords: Helicobacter pylori; cag pathogenicity island; NF-kappaB; PI3K/Akt signaling; gastric epithelial cells
Affiliations: Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan. 

Abstract:  Background: The inflammatory response in Helicobacter pylori-infected gastric tissue is mediated by cag pathogenicity island (PAI)-dependent activation of nuclear factor-kappaB (NF-kappaB). Phosphatidylinositol 3-kinase (PI3K)/Akt signaling is known to play a role in NF-kappaB activation, but little information is available on the relationship between H. pylori and PI3K/Akt signaling in gastric epithelial cells. We examined whether H. pylori activates Akt in gastric epithelial cells, the role of cag PAI in this process and the role of Akt in regulating H. pylori-induced NF-kappaB activation. Results: Phosphorylated Akt was detected in epithelial cells of H. pylori-positive gastric tissues. Although Akt was activated in MKN45 and AGS cells by coculture with cag PAI-positive H. pylori strains, a cag PAI-negative mutant showed no activation of Akt. H. pylori also induced p65 phosphorylation. PI3K inhibitor suppressed H. pylori-induced p65 phosphorylation and NF-kappaB transactivation, as well as interleukin-8 expression. Furthermore, transfection with a dominant-negative Akt inhibited H. pylori-induced NF-kappaB transactivation. Transfection with small interference RNAs for p65 and Akt also inhibited H. pylori-induced interleukin-8 expression. Conclusion: The results suggest that cag PAI-positive H. pylori activates Akt in gastric epithelial cells and this may contribute to H. pylori-mediated NF-kappaB activation associated with mucosal inflammation and carcinogenesis. 

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2021 04 15 pharma-company-demands-retraction-damages-in-lawsuit-against-journal for concerns about this article. ,
Generation of Powerful Human Tolerogenic Dendritic Cells by Lentiviral-Mediated IL-10 Gene Transfer
Authors: Silvia Gregori
Anna Kajaste-Rudnitski
Giada Amodio
Fabio Russo
Laura Passeri
Grazia Andolfi
Marta Fortunato
Luca Cesana
Francesca Romana Santoni de Sio
Michela Comi
Journal: Frontiers in Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: IL-10; allogeneic transplantation; cell therapy; dendritic cells; immune tolerance.
Affiliations: San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), San Raffaele Scientific Institute (IRCCS), Milan, Italy.

Abstract:  The prominent role of dendritic cells (DC) in promoting tolerance and the development of methods to generate clinical grade products allowed the clinical application of tolerogenic DC (tolDC)-based therapies for controlling unwanted immune responses. We established an efficient method to generate tolerogenic human DC, producing supra-physiological levels of IL-10, by genetically engineering monocyte-derived DC with a bidirectional Lentiviral Vector (bdLV) encoding for IL-10 and a marker gene. DCIL-10 are mature DC, modulate T cell responses, promote T regulatory cells, and are phenotypically and functionally stable upon stimulation. Adoptive transfer of human DCIL-10 in a humanized mouse model dampens allogeneic T cell recall responses, while murine DCIL-10 delays acute graft-vs.-host disease in mice. Our report outlines an efficient method to transduce human myeloid cells with large-size LV and shows that stable over-expression of IL-10 generates an effective cell product for future clinical applications in the contest of allogeneic transplantation. 

Retracted: No

PubPeer comments:
 Figure 1d is puzzling. Two images have areas of near identical appearance (cyan boxes) but also areas of differences (red boxes). Could the authors examine these images and explain? Further, the caption seems to only partially apply to the accompanying image. For example, I do not see a (b) or (c), nor any SD bars. Apologies if I am misunderstanding something. *** ![file] , 
 #1 This illustration may assist in showing the areas of overlap. *** ![file] ,
Inhibitors of pathogen intercellular signals as selective anti-infective compounds
Authors: Ronald G Tompkins
Sylvain Milot
Katie Padfield
Marie-Hélène Castonguay
A Aria Tzika
Scott Stachel
François Lépine
Qunhao Zhang
Laurence G Rahme
Eric Déziel
Biliana Lesic
Jiangwen Zhang
Journal: PLoS Pathogens (2007)
Discipline: MICROBIOLOGY
Keywords: Long-term antibiotic use; pan-resistant super pathogens; anti-infective compounds; virulence pathways; quorum sensing (QS)
Affiliations: Department of Surgery, Microbiology and Molecular Genetics, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts, USA.

Abstract:  Long-term antibiotic use generates pan-resistant super pathogens. Anti-infective compounds that selectively disrupt virulence pathways without affecting cell viability may be used to efficiently combat infections caused by these pathogens. A candidate target pathway is quorum sensing (QS), which many bacterial pathogens use to coordinately regulate virulence determinants. The Pseudomonas aeruginosa MvfR-dependent QS regulatory pathway controls the expression of key virulence genes; and is activated via the extracellular signals 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS), whose syntheses depend on anthranilic acid (AA), the primary precursor of 4-hydroxy-2-alkylquinolines (HAQs). Here, we identified halogenated AA analogs that specifically inhibited HAQ biosynthesis and disrupted MvfR-dependent gene expression. These compounds restricted P. aeruginosa systemic dissemination and mortality in mice, without perturbing bacterial viability, and inhibited osmoprotection, a widespread bacterial function. These compounds provide a starting point for the design and development of selective anti-infectives that restrict human P. aeruginosa pathogenesis, and possibly other clinically significant pathogens. 

Retracted: No

PubPeer comments:
 Figures 3B and 4C. Much more similar than expected. https: imgur.com epBDuZV , 
 Figure 5. Much more similar than expected. https: imgur.com rwDM1Z9 , 
 #2 I have communicated with the first author. He has provided the images from the original films (scanned this morning) which are available. He explained that same lysates were used for figures 4C, 5B and 5C, thus same actin. He acknowledged that this might not be crystal clear in the legends (his fault). For fig. 3B, he has at least three exposures available some of which are high exposures. He mentioned that the black dot that makes the figures suspicious is not present in any of the films. The dot is also present in some other figures and may be from the scanner. He has further acknowledged that the experiments were done in 2007 and 2008 and he could not recalled everything exactly. Moreover, he discarded most exposures (keeping one or two) during his relocation in 2017. Dong M. Shin , 
 ![file] ,
Long noncoding RNA MAPKAPK5-AS1 promotes colorectal cancer progression by cis-regulating the nearby gene MK5 and acting as a let-7f-1-3p sponge
Authors: Tao Jiang
Pei-Cong Shi
Hu Song
Ting Yang
Man-Ru Liu
Jia-Qi Wang
Rui-Zhi Fan
Wei-Cong Chen
Dong-Sheng Pei
Jun Song
Journal: Journal of Experimental & Clinical Cancer Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: CRC; Let-7f-1-3p; MK5; MK5-AS1; SNAI1.
Affiliations: Department of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, Jiangsu Province, China., Department of Pathology, Xuzhou Medical University, Xuzhou, 221002, Jiangsu Province, China., Department of Pathology, Xuzhou Medical University, Xuzhou, 221002, Jiangsu Province, China. ., Department of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, Jiangsu Province, China. ., Institute of Digestive Diseases of Xuzhou Medical University, Xuzhou, 221002, Jiangsu Province, China. .

Abstract:  Background: Long noncoding RNAs (lncRNAs) are considered critical regulators in cancers; however, the clinical significance and mechanisms of MAPKAPK5-AS1 (hereinafter referred to as MK5-AS1) in colorectal cancer (CRC) remain mostly unknown. Methods: In this study, quantitative real-time PCR (qPCR) and western blotting were utilized to detect the levels of MK5-AS1, let-7f-1-3p and MK5 (MAPK activated protein kinase 5) in CRC tissues and cell lines. The biological functions of MK5-AS1, let-7f-1-3p and MK5 in CRC cells were explored using Cell Counting Kit-8 (CCK8), colony formation and transwell assays. The potential mechanisms of MK5-AS1 were evaluated by RNA pull-down, RNA immunoprecipitation (RIP), dual luciferase reporter assay, chromatin immunoprecipitation (ChIP) and bioinformatics analysis. The effects of MK5-AS1 and MK5 on CRC were investigated by a xenotransplantation model. Results: We confirmed that MK5-AS1 was significantly increased in CRC tissues. Knockdown of MK5-AS1 suppressed cell migration and invasion in vitro and inhibited lung metastasis in mice. Mechanistically, MK5-AS1 regulated SNAI1 expression by sponging let-7f-1-3p and cis-regulated the adjacent gene MK5. Moreover, MK5-AS1 recruited RBM4 and eIF4A1 to promote the translation of MK5. Our study verified that MK5 promoted the phosphorylation of c-Jun, which activated the transcription of SNAI1 by directly binding to its promoter. Conclusions: MK5-AS1 cis-regulated the nearby gene MK5 and acted as a let-7f-1-3p sponge, playing a vital role in CRC tumorigenesis. This study could provide novel insights into molecular therapeutic targets of CRC. 

Retracted: No

PubPeer comments:
 Fig. 3E has a duplication, yet the one on the right seems a bit brighter. ![file] , 
 Two images in Fig. 7A overlap ![file] , 
 Figure 2A also. This lab appears to have some difficulty organizing their data. This might create concern about the reliability of their results. *** ![file] , 
 Another in 7A. *** ![file] ,
<p>Long Intergenic Non-Coding RNA 01121 Promotes Breast Cancer Cell Proliferation, Migration, and Invasion via the <em>miR-150-5p</em>/HMGA2 Axis</p>
Authors: Mengqi Zhang
Hong Yin
Fucheng Li
Pinghu Wang
Lin Cao
Duying Xie
Zhuolu Wang
Jing Zhu
Shenjia Duan
Xingchu Chen
Lin Guo
Guorong Yuan
Lixin Xiao
Journal: Cancer Management and Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: LINC01121; breast cancer; growth; invasion; miR-150-5p
Affiliations: Department of Breast Surgery, Hunan Provincial Maternal and Child Health Care Hospital, Changsha 410008, People's Republic of China., Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, People's Republic of China.

Abstract:  Purpose: Long intergenic noncoding RNA 01121 (LINC01121) has been reported to be aberrantly expressed and acts as an oncogene in pancreatic cancer. However, the detailed molecular mechanism of LINC01121 in breast cancer remains largely unclear. In this study, we aimed to investigate the expression and biological function of LINC01121 in breast cancer. Methods: LINC01121 and miR-150-5p expression were measured in breast cancer cell lines using quantitative reverse transcription PCR. MTS and ﬂow cytometry assays were performed to determine cell proliferation, the cell cycle, and apoptosis. Cell migration and invasion were assessed by transwell assay. The protein expression of HMGA2 in breast cancer cell lines was measured by Western blotting. A luciferase reporter assay was used to assess the binding of LINC01121 and miR-150-5p. Results: We found that LINC01121 was markedly up-regulated in breast cancer cell lines compared with normal breast epithelial cells. LINC01121 down-regulation markedly suppressed cell proliferation, cell cycle progression, migration, and invasion and promoted apoptosis in breast cancer cells. Further investigation showed that LINC01121 could serve as a molecular sponge for miR-150-5p and indirectly modulate the expression of its target, HMGA2. Moreover, miR-150-5p knockdown rescued the effects of LINC01121 down-regulation on HMGA2 protein expression, cell proliferation, cell cycle progression, apoptosis, migration, and invasion in breast cancer cells. Conclusion: Knockdown LINC01121 inhibited breast cancer cell proliferation, migration, and invasion via the miR-150-5p/HMGA2 axis. 

Retracted: No

PubPeer comments:
 Could the authors comment on the similarities between images c and d in Figure 3? *** ![file] , 
 Ag dots size increased within the rods , 
 #2 I think the first author misunderstood the question in the first comment. So, let me try to ask in a slightly different way: When comparing Figure 3C with Figure 3D, the rods are aligned in the same way in these two pictures. Figure 3D seems to be a slightly zoomed-in version of Figure 3C. Can the authors please check that Figure 3D and Figure 3C are not accidental duplicates of the same sample? , 
 #2 Thank you for your reply. To my eye, it appears that the image in d. has been stretched, which also explains how the u201c30nmu201d lettering in d. came to be distorted. ,