PReD-Bench/PRed-Bench huggingface dataset:
FGF10 Protects Against Renal Ischemia/Reperfusion Injury by Regulating Autophagy and Inflammatory Signaling
Authors: Hongmei Zhu
Xiaokun Li
Lisha Guo
Xiayu Wei
Jin-San Zhang
Qianyu Tao
Tianfang Jiang
Ruo Yang
Le Xu
Xiaohua Tan
Jin Wu
Journal: Frontiers in Genetics (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: FGF10; HMGB1; acute kidney injury; autophagy; inflammation
Affiliations: School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China., Qingdao University Medical College, Qingdao, China., The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China., Institute of Life Sciences, Wenzhou University, Wenzhou, China.

Abstract:  Ischemia-reperfusion (I/R) is a common cause of acute kidney injury (AKI), which is associated with high mortality and poor outcomes. Autophagy plays important roles in the homeostasis of renal tubular cells (RTCs) and is implicated in the pathogenesis of AKI, although its role in the process is complex and controversial. Fibroblast growth factor 10 (FGF10), a multifunctional FGF family member, was reported to exert protective effect against cerebral ischemia injury and myocardial damage. Whether FGF10 has similar beneficial effect, and if so whether autophagy is associated with the potential protective activity against AKI has not been investigated. Herein, we report that FGF10 treatment improved renal function and histological integrity in a rat model of renal I/R injury. We observed that FGF10 efficiently reduced I/R-induced elevation in blood urea nitrogen, serum creatinine as well as apoptosis induction of RTCs. Interestingly, autophagy activation following I/R was suppressed by FGF10 treatment based on the immunohistochemistry staining and immunoblot analyses of LC3, Beclin-1 and SQSTM1/p62. Moreover, combined treatment of FGF10 with Rapamycin partially reversed the renoprotective effect of FGF10 suggesting the involvement of mTOR pathway in the process. Interestingly, FGF10 also inhibited the release of HMGB1 from the nucleus to the extracellular domain and regulated the expression of inflammatory cytokines such as TNF-α, IL-1β and IL-6. Together, these results indicate that FGF10 could alleviate kidney I/R injury by suppressing excessive autophagy and inhibiting inflammatory response and may therefore have the potential to be used for the prevention and perhaps treatment of I/R-associated AKI. 

Retracted: No

PubPeer comments:
 Figure 6A. * Red boxes: The I R and RAPA panels appear to show an overlap. ![file] , 
 Corrigendum, November 2021: https: www.frontiersin.org articles 10.3389 fgene.2021.731406 full  In the original article, there were mistakes in Figure 2A, Figure 6A, and Figure 7A as published. The immunofluorescence and immunohistochemistry images in the Sham group (Figure 2A) and RAPA groups in Figure 6A and Figure 7A, respectively, were erroneously used. The corrected Figures appear below. The authors deeply apologize for these errors and state that these corrections do not change the scientific conclusions of the article in any way. The original article has been updated. ,
Effects of miR-132 on proliferation and apoptosis of pancreatic cancer cells via Hedgehog signaling pathway
Authors: F-B Sun
B Han
Y-S Hou
D-W Zhao
S-J Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miRNAs; Hedgehog signaling pathway; pancreatic cancer cells; proliferation; apoptosis
Affiliations: Department of Gastrointestinal Surgery, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. .

Abstract:  Objective: Micro ribonucleic acids (miRNAs) and Hedgehog (Hh) signaling pathway play key roles in the proliferation, migration and invasion of tumor cells. The aim of this study was to investigate the role of miR-132 and Hh signaling pathway in the proliferation and apoptosis of pancreatic cancer cells, and to investigate the possible underlying mechanism. Materials and methods: The expressions of miR-132 and Shh (a ligand of Hh) in clinical pancreatic cancer specimens and pancreatic cancer cell lines were determined by qRT-PCR. Meanwhile, the correlation between the two molecules was analyzed. Pancreatic cancer cell line (MiaPaCe-2a) was transfected with miR-132 mimics and inhibitor. The effects of miR-132 up- and down-regulation on the expressions of miR-132, Shh, Cyclin-D1, cleaved Caspase-3 and cleaved Caspase-9 were detected. In addition, the exact role of miR-132 in the proliferation, apoptosis and distribution of MiaPaCe-2a cells were investigated. Results: The expression level of miR-132 in pancreatic cancer specimens and pancreatic cancer cell lines was significantly elevated when compared with that of control group. Meanwhile, miR-132 expression was negatively correlated with the expression level of Shh. Moreover, transfection with miR-132 mimics evidently up-regulated miR-132 expression. Moreover, miR-132 up-regulation significantly decreased the mRNA and protein expressions of Shh, facilitated the proliferation of MiaPaCe-2a cells, reduced the protein expressions of Cyclin-D1, cleaved Caspase-3 and cleaved Caspase-9, and suppressed cell apoptosis. On the contrary, miR-132 inhibitor transfection significantly inhibited the proliferative activity of MiaPaCe-2a cells, decreased the proportion of cells in G1 phase, and increased the proportion of cells in G2/M phase. Conclusions: MiR-132 promotes proliferation and inhibits apoptosis of pancreatic cancer cells through Hh signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 3E shows three different flow cytometry plots, but some parts of these three plots look more similar than expected. Rounded boxes of the same color bring attention to parts that look very similar. ![file] ,
Combination Treatment of Icariin and L-DOPA Against 6-OHDA-Lesioned Dopamine Neurotoxicity
Authors: Ya-Xin Zheng
Guo-Qing Wang
Dai-Di Li
Ce Chen
Jie Liu
Jingshan Shi
Feng Zhang
Di-Sheng Lu
Journal: Frontiers in molecular neuroscience (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Icariin; L-DOPA; Parkinson’s disease; combination treatment; dyskinesia.
Affiliations: Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, China.

Abstract:  Until now, the dopamine (DA) precursor, L-3,4-dihydroxyphenylalanine (L-DOPA), remains the gold standard effective drug therapy for Parkinson's disease (PD) patients. Nevertheless, long-term chronic L-DOPA administration leads to the drug efficacy loss and severe adverse effects, such as L-DOPA-induced dyskinesia (LID). Icariin (ICA), a flavonoid that is extracted from Epimedium, has been proved to evoke neuroprotection against DA neuronal loss in PD animal models. Here, the present study detected the effects of ICA combined with L-DOPA on 6-hydroxydopamine (6-OHDA)-elicited DA neurotoxicity and L-DOPA-induced motor dysfunction as well. PC12 cells were applied to investigate the combination treatment of ICA and L-DOPA against 6-OHDA-lesioned neurotoxicity. In addition, rat substantia nigral stereotaxic injection of 6-OHDA-induced DA neuronal injury was performed to explore the neuroprotective effects mediated by ICA combined with L-DOPA. The pathological movement triggered by L-DOPA was determined by the abnormal involuntary movements (AIM) scores analysis. In PC12 cells, ICA combined with L-DOPA produced better neuroprotection from 6-OHDA-induced neurotoxicity than ICA or L-DOPA alone treatment. In parkinsonian 6-OHDA lesioned rats, ICA conferred DA neuroprotection as monotherapy and an enhancement benefit of L-DOPA treatment after daily administration of L-DOPA and ICA for 21 days. Moreover, ICA ameliorated the development of LID as evidenced by the lowered AIM scores without affecting L-DOPA-mediated efficacy. Furtherly, ICA attenuated neuroinflammation in 6-OHDA-induced DA neuronal loss and the development of LID in vivo. In conclusion, these findings suggest ICA might be a potential promising adjuvant to enhance L-DOPA efficacy and attenuate L-DOPA-produced adverse effects in PD. 

Retracted: No

PubPeer comments:
 This paper has several problems: 1) Coordinates are not provided which makes it impossible to check reproduce. 2) If one follows the IRCs from transition states shown in Figure 2 they will end up with different reactants than what the authors propose. The BeH2 will be coordinated to the 1,3-dipole and the overall reaction will become thermodynamically unfavored. 3) The coordination of BeH2 to the dipole is favored over any shown geometries, the proposed reactions won t happen. ,
A role for extrarenal cells in the regeneration following acute renal failure
Authors: Sandeep Gupta
Mark E Rosenberg
Catherine Verfaillie
Youngki Kim
David Chmielewski
Journal: Kidney International (2002)
Discipline: CLINICAL MEDICINE
Keywords: Renal function; Acute tubular necrosis; Stem cells; Recovery; Organ injury
Affiliations: Division of Renal Diseases and Hypertension, Department of Medicine, University of Minnesota, 516 Delaware Street S.E., Minneapolis, MN 55455, USA.

Abstract:  Background: Recovery of renal function following acute tubular necrosis (ATN) is dependent on the replacement of necrotic tubular cells with functional tubular epithelium. The source of these new tubular cells is thought to be resident renal tubular cells. The discovery of pluripotent bone marrow-derived stem cells has led to a reexamination of the cellular source and processes involved in the recovery from organ injury. Methods: To test the hypothesis in humans that extrarenal cells participate in the recovery following ATN, we examined the origin of tubular cells in male patients with resolving ATN who had received a kidney transplant from a female donor. Immunohistochmistry of kidney biopsies was performed to identify renal tubular epithelial cells (cytokeratin positive) and leukocytes (CD45 positive). Fluorescent in-situ hybridization was used to detect Y chromosome containing cells with DAPI serving as a nuclear stain. All staining was performed on the same section. Results: The Y chromosome was detected in approximately 40% of tubular cell nuclei in male kidneys (positive control) and in no nuclei of female kidneys (negative control). In male recipients of female kidneys who developed ATN, 1% of tubules contained Y chromosome cells defined by their morphology, positive staining for cytokeratin, and negative staining for CD45. When present, multiple cells in a positive tubule stained for the Y chromosome. No Y chromosome containing tubular cells were seen in similar sex mismatched transplants in male recipients who did not develop ATN, suggesting that recipient derived cells do not routinely repopulate the transplanted kidney. Conclusions: This proof-of-principle clinical observation demonstrates that extrarenal cells can participate in the regenerative response following ATN. These findings provide rationale for the cellular therapy of acute renal failure. 

Retracted: No

PubPeer comments:
 Figure 1. This figure is used to demonstrate that transplanted kidneys are regenerated with extrarenal (from the recipient for the kidney) cells. Red dye depicts position of Y chromosomes in donor kidney tissue. * Marked with yellow boxes: Panels A (male recipient of male kidney) and D (male recipient of female kidney) look very similar if one of the two panels is rotated 180 degrees. Both show the presence of Y chromosomes (red dots). ![file] Here is a side-by-side comparison of panels A and rotated panel D. ![file] ,
MNNG-induced cell death is controlled by interactions between PARP-1, poly(ADP-ribose) glycohydrolase, and XRCC1
Authors: Tina Gröbe
Claudia Keil
Shiao Li Oei
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PARP-1; poly(ADP-ribose); PARG; XRCC1; genomic stability
Affiliations: Institut für Biochemie, Freie Universität Berlin, Thielallee 63, 14195 Berlin, Federal Republic of Germany.

Abstract:  PARP-1 (poly(ADP-ribose) polymerases) modifies proteins with poly(ADP-ribose), which is an important signal for genomic stability. ADP-ribose polymers also mediate cell death and are degraded by poly(ADP-ribose) glycohydrolase (PARG). Here we show that the catalytic domain of PARG interacts with the automodification domain of PARP-1. Furthermore, PARG can directly down-regulate PARP-1 activity. PARG also interacts with XRCC1, a DNA repair factor that is recruited by DNA damage-activated PARP-1. We investigated the role of XRCC1 in cell death after treatment with supralethal doses of the alkylating agent MNNG. Only in XRCC1-proficient cells MNNG induced a considerable accumulation of poly(ADP-ribose). Similarly, extracts of XRCC1-deficient cells produced large ADP-ribose polymers if supplemented with XRCC1. Consequently, MNNG triggered in XRCC1-proficient cells the translocation of the apoptosis inducing factor from mitochondria to the nucleus followed by caspase-independent cell death. In XRCC1-deficient cells, the same MNNG treatment caused non-apoptotic cell death without accumulation of poly(ADP-ribose). Thus, XRCC1 seems to be involved in regulating a poly(ADP-ribose)-mediated apoptotic cell death. 

Retracted: No

PubPeer comments:
  Figure 8. H E stained splanchnic slices 30 days after the injection of AuNR@CuPDA. The control group is age-matched healthy mice. The thermochemotherapy group is AuNR@CuPDA by i.v. + laser group in our experiments. ![file] Control and Treatment slices for spleen appear to be overlapping segments of a single larger image. ![file] , 
 At left, Figure 5:  **(au2212c) T1-weighted MRI of nude mice bearing KB tumor without AuNR@CuPDA treatment**. (du2212f) T1-weighted MRI of mice 24 h after the injection of 50 u03bcL 50 u03bcg mL AuNR@CuPDA solution. (gu2212i) T1-weighted MRI of mice 7 days after the treatment. At right, Figure 7 from [Li et al (2018)] :  (Figure C-F) The MRI after the injection of NPs. **(Figure G-J) The MRI before the injection of NPs** . ![file] , 
 Figure 6: Two mice share many similarities with mice presented in Figure Some tumor images are identical between the two papers. In addition, the presentation of tumor growth is similar. ![file] ![file] , 
 Figure 6: an image of a mouse and tumors are reused in another paper (Ge, R et al., 2017; ![file] ) ![file] , 
 The reused images between different two papers represent different experiment conditions. Interestingly, one mouse images were labeled with roman numerals I II III IV, while the other mouse were labeled with arabic numerals 1 2 3 4. ![file] ,
The positive feedback between lncRNA TNK2-AS1 and STAT3 enhances angiogenesis in non-small cell lung cancer
Authors: Dongmei Han
Yue Wang
Jing Sun
Liming Pan
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: NSCLC; STAT3; TNK2-AS1; VEGFA.
Affiliations: Department of Thoracic Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, 130033, China., Department of Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, 130033, PR China., The First Hospital of Jilin University, Changchun, Jilin Province, 130021, China., Health Examination Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, 130033, China. Electronic address: .

Abstract:  Evidence has shown the importance of long non-coding RNAs (lncRNAs) during angiogenesis and lung cancer progression. However, the potential functions of TNK2-AS1 in non-small cell lung cancer (NSCLC) remain elusive. By lncRNA profiling, we identified TNK2-AS1 as a novel oncogenic lncRNA in NSCLC. TNK2-AS1 was significantly upregulated in NSCLC and correlated with poor prognosis. We found that TNK2-AS1 could increase viability and migration of NSCLC cells in vitro. TNK2-AS1 also promoted NSCLC xenograft tumor growth and metastasis in vivo. TNK2-AS1 could interact with STAT3 to increase its protein stability by protecting it from proteasome-mediated degradation. STAT3 could also bind TNK2-AS1 promoter to trigger its transcription. The positive feedback loop between STAT3 and TNK2-AS1 therefore augmented STAT3 signaling by elevating VEGFA expression to facilitate angiogenesis. Collectively, our work has elucidated a novel mechanism of TNK2-AS1-mediated angiogenesis by enforcing STAT3/VEGFA signaling and may provide a potential target for therapeutic intervention. 

Retracted: No

PubPeer comments:
 Two images in Figure 3F showing no signal appear to be the same. Could the authors please provide the original uncropped scans? I did not check elsewhere. *** ![file] ,
microRNA-1225 inhibit apoptosis of pancreatic cancer cells via targeting JAK1
Authors: Liu Yang
Li Wang
Kaifeng Fang
Sheng Li
Ruolei Zhong
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: JAK1; Pancreatic cancer; apoptosis; miR-1225-5p.
Affiliations: a Cancer Center, Union Hospital, Tongji Medical College , Huazhong University of Science and Technology , Wuhan , China., b Department of General Surgery , The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University , Wuhan , China., c Department of General Surgery , Hosiptal of Huazhong University of Science and Technology , Wuhan , China., d Department of Emergency Surgery, Union Hospital, Tongji Medical College , Huazhong University of Science and Technology , Wuhan , China., e Department of Dermatology, Union Hospital, Tongji Medical College , Huazhong University of Science and Technology , Wuhan , China.

Abstract:  The microRNA miRNA-1225-5p (miR-1225) is known as an essential modulator of the development of multiple cancers and other biological reactions. However, the understanding of its contribution to pancreatic cancer (PC) is insufficient. The effects of miR-1225 on PC cell survival and tumorigenesis in vivo as well as on the modulation of cell apoptosis were investigated. The expression of miR-1225 was upregulated in 20 human LC samples from acute myeloid leukemia patients with adverse prognosis and poor responses to therapy as well as in several human PC cell lines, as compared to that in healthy tissues, normal tissues, and normal pancreatic cells. In contrast, Janus kinase 1 (JAK1) expression was downregulated in human-derived PC samples and PC cell lines. EdU staining demonstrated that the aberrant expression of miR-1225 impaired the proliferation and survival of these two PC cell lines. The depletion of miR-1225 expression increased the apoptosis of both PANC-1 and AsPC-1 cells, as revealed by the TdT-mediated dUTP nick end labeling (TUNEL) staining and flow cytometry results. The results of dual-luciferase reporter assay indicated that miR-1225 targeted the 3'-untranslated region of JAK1 for silencing. Silencing of JAK1 expression counteracted the suppressive influence of miR-1225 depletion in PC cells. Thus, these results offer an insight into the biological and molecular mechanisms underlying the development of PC and provide potential strategies for PC treatment. 

Retracted: No

PubPeer comments:
 In Figure 6A and B, two Western immunoblot panels have been duplicated and presented as something else. Caspase-3 vs JAK1. ![file] ,
Disease-regulated local IL-10 gene therapy diminishes synovitis and cartilage proteoglycan depletion in experimental arthritis
Authors: Onno J Arntz
Peter L E M van Lent
Marije I Koenders
Mathijs G A Broeren
Eline A Vermeij
Fons A J van de Loo
Wim B van den Berg
Miranda B Bennink
Inger Gjertsson
Journal: Annals of the Rheumatic Diseases (2015)
Discipline: CLINICAL MEDICINE
Keywords: Arthritis; Cytokines; Inflammation; Synovitis; Treatment.
Affiliations: Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands., Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.

Abstract:  Objectives: Rheumatoid arthritis is a chronic destructive autoimmune disease, but the course is unpredictable in individual patients. An attractive treatment would provide a disease-regulated therapy that offers personalised drug delivery. Therefore, we expressed the anti-inflammatory interleukin-10 (IL-10) gene under the control of inflammation-dependent promoters in a mouse model of arthritis. Methods: Proximal promoters of S100a8, Cxcl1, Mmp13, Saa3, IL-1b and Tsg6 were selected by whole-genome expression analysis of inflamed synovial tissues from arthritic mice. Mice were injected intraarticularly in knee joints with lentiviral vectors expressing a luciferase reporter or the therapeutic protein IL-10 under control of the Saa3 or Mmp13 promoter. After 4 days, arthritis was induced by intraarticular injection of streptococcal cell walls (SCW). At different time points after arthritis induction, in vivo bioluminescent imaging was performed and knee joints were dissected for histological and RNA analysis. Results: The disease-regulated promoter-luciferase reporter constructs showed different activation profiles during the course of the disease. The Saa3 and Mmp13 promoters were significantly induced at day 1 or day 4 after arthritis induction respectively and selected for further research. Overexpression of IL-10 using these two disease-inducible promoters resulted in less synovitis and markedly diminished cartilage proteoglycan depletion and in upregulation of IL-1Ra and SOCS3 gene expression. Conclusions: Our study shows that promoters of genes that are expressed locally during arthritis can be candidates for disease-regulated overexpression of biologics into arthritic joints, as shown for IL-10 in SCW arthritis. The disease-inducible approach might be promising for future tailor-made local gene therapy in arthritis. 

Retracted: No

PubPeer comments:
 Fig 4, images in panels in yellow box are same while treatments are different. ![file] ,
Stearoyl-CoA Desaturase 1 Potentiates Hypoxic plus Nutrient-Deprived Pancreatic Cancer Cell Ferroptosis Resistance
Authors: Dongqing Wang
Zining Zhang
Aihua Gong
Zhengyang Zhang
Ming Wang
Xiang Liao
Haitao Zhu
Jie Gao
Lin Xia
Yanfang Liu
Journal: Oxidative Medicine and Cellular Longevity (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hypoxia; nutrient starvation; pancreatic carcinoma; ferroptosis resistance; lipid compositions
Affiliations: Department of Medical Imaging, The Affiliated Hospital of Jiangsu University, Zhenjiang, China 212001., School of Medicine, Jiangsu University, Zhenjiang, China 212013., International Genome Center, Jiangsu University, Zhenjiang, China 212013.

Abstract:  Hypoxia and nutrient starvation (H/NS) microenvironment, a notable characteristic of pancreatic carcinoma, plays a critical role in cell death resistance and tumor recurrence. However, its role in ferroptosis remains to be classified. Here, we found that H/NS contributed to the pancreatic cancer cell ferroptosis resistance depending on the altered intracellular lipid compositions. Mechanistically, H/NS induced the upregulation of stearoyl-CoA desaturase 1 (SCD1), which promoted monounsaturated fatty acids (MUFAs) synthesis and protected against lipid peroxidation. Surprisingly, SCD1 showed a strong correlation with antiferroptosis gene expression. Moreover, short-hairpin RNA-based knockdown of SCD1 enhanced erastin-induced ferroptosis in vitro under H/NS. Finally, our results demonstrate the synergistic effect of erastin and A939572, a special SCD1 inhibitor, in dictating pancreatic carcinoma subcutaneous ferroptotic death. Taken together, our findings reveal a new role of the H/NS microenvironment against ferroptosis and suggest a potential therapeutic strategy for overcoming ferroptosis resistance in pancreatic cancer cells. 

Retracted: Yes

PubPeer comments:
 Figure 1b has a problem: two cases of data duplication. ![file] , 
 Retraction, February 2022, found here: https: www.hindawi.com journals omcl 2022 9809570  Oxidative Medicine and Cellular Longevity has retracted the article titled u201cStearoyl-CoA Desaturase 1 Potentiates Hypoxic plus Nutrient-Deprived Pancreatic Cancer Cell Ferroptosis Resistanceu201d [1] due to concerns with figure duplications in Figure 1(b) as originally noted on PubPeer [2]. Specifically, the DMSO Nor panel is duplicated with the DMSO H NS panel, and the Erastin Nor+Fer-1 panel is duplicated with the SAS Nor+Fer-1 panel. In both cases, the field of view is different between the panels. The author responded to explain that the duplications were introduced due to an error when preparing their manuscript, however, this did not satisfy the concerns of the editorial board and the article is retracted due to concerns with the reliability of the data. The authors do not agree to the retraction. ,
Human papillomavirus type 77 E6 protein selectively inhibits p53-dependent transcription of proapoptotic genes following UV-B irradiation
Authors: Ramon García-Escudero
Judith Green
Alan Storey
Silvia Giampieri
Journal: Oncogene (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA damage; UV-B; p53 protein; apoptosis; oncogenic anogenital human papillomaviruses
Affiliations: Cancer Research UK, Skin Tumour Laboratory, 2 Newark Street, London E1 2AT, UK.

Abstract:  DNA damage, such as that elicited by UV-B, can induce either a cell cycle arrest or apoptosis that can be signalled by the p53 protein through the activation of a number of downstream cellular target genes. In contrast to oncogenic anogenital human papillomaviruses (HPVs), which mediate proteolytic degradation of p53, the E6 protein of cutaneous HPVs, such as HPV 77, do not promote p53 degradation. We have previously shown, however, that expression of HPV 77 E6 can effectively block UV-induced apoptosis in cells that have UV-activated p53. Here, we report that expression of the E6 protein from the cutaneous HPV 77 attenuates the UV-induced transactivation of p53-regulated proapoptotic genes Fas, PUMAbeta, Apaf-1, PIG3. This inhibition of p53-activation of proapoptotic genes by HPV77 E6 is exerted selectively, as the increased expression of p53 target genes involved in cell cycle arrest or regulatory functions regulation, such as p21 and Hdm2, is unaffected. Our data suggest that HPV 77 E6 may play an important role in specifically deregulating p53-dependent transactivation of proapoptotic genes upon UV-B irradiation. 

Retracted: No

PubPeer comments:
null, 
 This paper is included in a published literature review: Driscoll, S. K., Kulacki, K. and Marzooghi, S. (2019), A Review of the Literature on Potential Effects of Runoff from Refined Coalu2010Taru2010Based Sealant Coating on Aquatic Organisms. Integr Environ Assess Manag. Accepted Author Manuscript. doi:10.1002 ieam.4210 ,
Determining the Interfacial Refractive Index via Ultrasensitive Plasmonic Sensors
Authors: Zhong-Qun Tian
Chao Zhan
Bo-Wen Liu
Bin Ren
Journal: Journal of the American Chemical Society (2020)
Discipline: CHEMISTRY
Keywords: Plasmonic sensors; chemical analysis; biological analysis; experimental findings; theoretical calculations
Affiliations: State Key Laboratory of Physical Chemistry of Solid Surfaces, College of Chemistry and Chemical Engineering, Collaborative Innovation Center of Chemistry for Energy Materials (iChEM), Xiamen University, Xiamen 361005, China., College of Chemistry and Chemical Engineering, Lanzhou University, Lanzhou 730000, China.

Abstract:  Plasmonic sensors are promising for ultrasensitive chemical and biological analysis. However, there are increasing experimental findings that cannot be well addressed by theoretical calculations, including the nonlinear dependence of the plasmonic peak wavelength on the refractive index (RI) and the ultrahigh sensitivity beyond the theoretical limit. The gap between experiments and theoretical calculations is that the bulk RI (BRI) used for calculation could be different from the interfacial RI (IRI) determining the electromagnetic response as a result of the interaction of molecules with the surface. But there is still no method to determine the IRI. Herein, we quantitatively determine the IRI by disentangling the surface RI (SRI) from the BRI. The obtained IRI can be directly applied in theoretical calculations to reliably reflect the experimental response and rigorously guide the design of plasmonic sensors. Moreover, it can be a fundamental dimensionless number to describe the light-matter interaction at the interface. 

Retracted: No

PubPeer comments:
 Dear Authors Your paper says that  we discovered that surface adsorption plays a crucial role in high-sensitive detection of analyte . Normally, surface binding is quantified by a charcteristic extension length for the evanescent field, which dates back to Jung et al. Quantitative interpretation of the response of surface plasmon resonance sensors to adsorbed films (Langmuir 1998) I was wondering if you characterized the field extension for your structures, using for instance layer by layer deposition? Also, the adsorption of glycerol seems to contradict many previous studies which only observe a linear response from increased concentration, i.e. the linear response coincides with the initial resonance wavelength for pure water. I was wondering if there is any support in the literature for glycerol accumulating on gold surfaces? ,
Down‐regulated lncRNA SBF2‐AS1 in M2 macrophage‐derived exosomes elevates miR‐122‐5p to restrict XIAP, thereby limiting pancreatic cancer development
Authors: Zi Yin
Yu Zhou
Ning Shi
Sheng Chen
Yiping Zou
Tingting Ma
Chuanzhao Zhang
Baohua Hou
Journal: Journal of Cellular and Molecular Medicine (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LncRNA SBF2-AS1; MicroRNA-122-5p; X-linked inhibitor of apoptosis protein; exosomes; macrophages
Affiliations: General Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China., Obstetrics and Gynecology Department, Sun Yat-Sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.

Abstract:  Evidence has indicated that M2 macrophages promote the progression of cancers, but few focus on the ability of M2 macrophage-derived exosomes in pancreatic cancer (PC). This study aims to explore how M2 macrophages affect malignant phenotypes of PC through regulating long non-coding RNA SET-binding factor 2 antisense RNA 1 (lncRNA SBF2-AS1)/microRNA-122-5p (miR-122-5p)/X-linked inhibitor of apoptosis protein (XIAP) axis. THP-1 cells were transformed into M1 macrophages by lipopolysaccharide and interferon-γ treatment, and into M2 macrophages after interleukin-4 treatment. The PANC-1 PC cell line with the largest lncRNA SBF2-AS1 expression was selected, and M2 macrophage-derived exosomes were isolated and identified. A number of assays were applied for the examination of lncRNA SBF2-AS1 expression, PC cell biological functions and subcellular localization of lncRNA SBF2-AS1. XIAP expression was detected, along with the interaction among lncRNA SBF2-AS1, miR-122-5p and XIAP. M2 macrophage exosomal lncRNA SBF2-AS1 expression's effects on the tumorigenic ability of PANC-1 cells in nude mice were also investigated. M2 macrophage-derived exosomes promoted progression of PC cells. Overexpressed lncRNA SBF2-AS1 promoted progression of PC cells. LncRNA SBF2-AS1 was found to act as a competing endogenous RNA to repress miR-122-5p and up-regulate XIAP. Constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes contributed to restraining tumorigenic ability of PC cells. Collectively, our study reveals that constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes increases miR-122-5p expression to restrain XIAP expression, which further inhibits PC progression. 

Retracted: No

PubPeer comments:
 The paper **reproduces VERBATIM ~70% of ALL the text** in Advance Space Research 20, 1997 The chemistry of the ions 40 amu in the inner coma of the comet Halley. ![file] ![file] ![file] ,
Acupuncture and weight loss in Asians: A PRISMA-compliant systematic review and meta-analysis
Authors: Ying Chen
Ying Li
Zhiqiong He
Yunzhou Shi
Lin Zhang
Mingmin Xu
Junpeng Yao
Journal: Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: Acupuncture; body weight reduction; Asians; systematic review; meta-analysis
Affiliations: Chengdu University of Traditional Chinese Medicine., The Third Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Diabetes Mellitus Prevention and Control Center of Sichuan Province, Chengdu, Sichuan, People's Republic of China.

Abstract:  Background: Acupuncture is effective for reducing body weight; however, evidence in Asian populations is lacking. We performed a systematic review and meta-analysis to evaluate the efficacy of acupuncture for body weight reduction in Asians. Methods: The Medline, Embase, Cochrane library, and Chinese databases were searched for relevant studies through October 20, 2018. Publications describing randomized controlled trials (RCTs) comparing acupuncture with other treatments for the reduction of body weight were compiled. Reviewers assessed bias and collected data on trial characteristics and outcomes. The study was conducted based on the reporting items of the guidelines for systematic evaluation and meta-analysis (PRISMA). Review Manager 5.2 software was used to calculate weight mean difference (WMD) and 95% confidence intervals (CIs). Results: Twelve RCTs involving 1151 subjects were included. Compared with the control groups, the acupuncture groups exhibited significantly greater reductions of body mass index (BMI)(WMD -1.20kg/m2; 95% CI -1.91, -0.48)and waist circumference (WMD -1.85 cm; 95% CI -3.20, -0.49) In the subgroup analyses, significant differences in the reduction of BMI was observed between the acupuncture and sham acupuncture groups, the acupuncture plus diet and exercise, and the diet and exercise groups, and the acupuncture and no intervention groups, but not between the acupuncture plus exercise and exercise groups [corrected]. Conclusions: Our study demonstrates that acupuncture is effective in the intervention of overweight/obesity in Asians; however, compared with exercise alone, acupuncture combined with exercise had no effect on the BMI or waist circumstance in the short term. Long-term studies are needed to evaluate the efficacy of acupuncture in weight reduction in Asians. 

Retracted: No

PubPeer comments:
 See https: journals.lww.com md-journal Blog MedicineCorrespondenceBlog pages post.aspx?PostID=110 ,
Oridonin induces growth inhibition and apoptosis in human gastric carcinoma cells by enhancement of p53 expression and function
Authors: Jingtao Wang
Aihua Wang
Youxi Li
Dengqiang Liu
Xuying Mao
Enxu Bi
Journal: Brazilian Journal of Medical and Biological Research (2018)
Discipline: CLINICAL MEDICINE
Keywords: oridonin; gastric cancer; SNU-216; cell proliferation; cell migration
Affiliations: Qingdao West Coast New Area Central Hospital,  China, Affiliated Hospital of Qingdao University,  China

Abstract:  The tumor suppressive role of oridonin, an active compound extracted from Rabdosia rubescens, has been proven in several gastric cancer (GC) cell lines. The present study aimed to evaluate the effect of oridonin on another GC cell line, SNU-216, and explore the potential mechanisms. The viable cell numbers, cell migration, survival fraction, and cell viability were, respectively, evaluated by trypan blue exclusion assay, wound healing assay, clonogenic assay, and CCK-8 assay. Cell apoptosis was determined by flow cytometry assay and western blot. The expression of p53 was inhibited by transient transfection, and the efficiency was verified by western blot. qRT-PCR was performed to measure the mRNA expression of p53. Western blot was used to evaluate the protein expression of apoptosis, DNA damage and p53 function related factors. We found that oridonin significantly inhibited cell proliferation, migration, and survivability, and enhanced cell apoptosis in SNU-216 cells. However, it had no influence on HEK293 cell viability. Oridonin also remarkably enhanced the anti-tumor effect of cisplatin on SNU-216 cells, as it significantly increased apoptotic cells and decreased cell viability. Moreover, the mRNA and protein expression of p53 was significantly up-regulated in oridonin-treated cells, while Mdm2 expression was down-regulated. Furthermore, oridonin enhanced p53 function and induced DNA damage. Knockdown of p53 or employing the caspase inhibitor, Boc-D-FMK, reversed the effect of oridonin on cell viability and apoptosis-related protein expression. The present study demonstrated that oridonin exhibited an anti-tumor effect on GC SNU-216 cells through regulating p53 expression and function. 

Retracted: No

PubPeer comments:
 ![file] This paper conforms to a style identified by [Dr Elisabeth Bik] and [Dr Jana Christopher] , among others. ,
Effects of lentivirus-mediated silencing of Periostin on tumor microenvironment and bone metastasis via the integrin-signaling pathway in lung cancer
Authors: Jing Che
Peng Zhang
Wen-Zhuang Shen
Xiang-Lin Yuan
Yu Deng
Yong-De Liao
Yu-Hong Dai
Journal: Life Sciences (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bone metastasis; Integrin; Lung cancer; Periostin; Signaling pathway
Affiliations: Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China; College of Life Sciences, Wuhan University, Wuhan 430072, PR China., Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China., Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China., Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China., Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, 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 Figures 1B, 3B, 5B, and 8A which appear to have a similar phenotype as seen in many other publications, as detailed here: https://pubpeer.com/publications/E266A07D28435DB334E8777CAC97E3; and here: https://docs.google.com/spreadsheets/d/1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY/edit#gid=262337249. In addition, a portion of Figure 6B, ‘NC’ group appears to contain image similarities with Figure 6B, ‘si-Integrin-αvβ3’ group, and a portion of Figure 6B, ‘Blank’ group appears to contain image similarities with Figure 6B, ‘NC’ group. The journal requested that the corresponding author comment on these concerns and provide the raw data. However, the authors were not able to satisfactorily fulfill this request and therefore the Editor-in-Chief decided to retract the article. 

Retracted: No

PubPeer comments:
  Fig. 5. Spectral bioimaging analysis for internalization studies of various formulations into the dendritic cells: (a) mock-treated DCs, (b) plain liposomes-treated DCs, (c) OPM-coated liposomes-treated DCs.  Three of the five dendritic cells in (a) are the same, at different sizes and rotations. One of the cells in (c) is within a rectangle with a darker background from the rest of the image, and is apparently an inset from a different image. ![file] , 
  Fig. 2. AFM image of OPM-coated and-uncoated liposomes: (a) Plain liposomes, and (b) OPM-coated liposomes.  (a) and (b) are the same AFM image with different reproduction quality. ![file] ,
Fatal Adverse Events Associated With Programmed Cell Death Ligand 1 Inhibitors: A Systematic Review and Meta-Analysis
Authors: Tingting Zhuang
Xuewen Wang
Linbin Lu
Shijie Wu
Xiong Chen
Erqian Shao
Yaying Chen
Journal: Frontiers in Pharmacology (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PD-L1 inhibitors; fatal adverse events; incidence; interstitial lung disease; meta-analysis.
Affiliations: Department of Oncology, The 900th Hospital of the People's Liberation Army Joint Service Support Force, Fuzong Clinical Medical College of Fujian Medical University, Fuzhou, China., Department of Clinical Medicine, Fujian Medical University, Fuzhou, China.

Abstract:  Purpose: We performed this systematic review and meta-analysis to assess the incidence of fatal adverse events that were associated with the use of programmed cell death ligand 1 (PD-L1) inhibitors, to describe them and to statistically depict factors that were associated with these events. Method: PubMed, Embase, and Cochrane Library were completely searched based on the following terms or relevant Medical Subject Heading ones: "atezolizumab", "durvalumab", "avelumab", and "cemiplimab". Results: A total of 26 eligible studies were identified, incorporating 6,896 unique participants. The overall incidence was 1.24% (95% CI: 0.93-1.65%). The incidence and odds were higher in patients with non-squamous non-small cell lung cancer (NSCLC) than those with urothelial carcinoma [(2.25 vs. 0.85, p = 0.04), (odds ratio [OR]: 2.69; 95% CI: 1.04-6.97, p = 0.04)], higher in the middle-aged group than the young group [(1.74 vs. 0.89, p = 0.01), (OR: 2.13; 95% CI: 1.26-3.61, p = 0.01)], and higher in the trial phase I than the trial phase II [(1.76 vs. 0.60, p = 0.01), (OR: 0.31; 95% CI: 0.13-0.75, p = 0.01)]. Notably, the trial phase I had a higher incidence than trial phase II or III following regulating for cancer types and average age (OR: 0.28; 95% CI: 0.11-0.71, p = 0.01, OR: 0.48; 95% CI: 0.24-0.95, p = 0.04, respectively). In terms of organ-specific fatal adverse events, interstitial lung disease (ILD) was frequently documented. A variety of respiratory system-related fatal adverse events were recorded, including but not limited to pneumonia and respiratory failure. As for organ-unspecific fatal adverse events, substantial cases of sepsis and neutropenia were recorded. Conclusion: This study firstly provided a comprehensive incidence and the spectrum of fatal adverse events associated with PD-L1 inhibitors, and identified three potential susceptible factors of that, yielding a capability for clinicians to distinguish high-risk populations from relatively low-risk ones, and facilitating to improve the safety of PD-L1 inhibitors broadly used in the clinical setting. 

Retracted: No

PubPeer comments:
 The text refers four times to a  Begger s Test . E.g., * However, there was no evidence to prove publication bias existed in this study based on Beggeru2019s test (p = 0.57). Moreover, when 26 eligible studies and 44 ineligible ones were included in the analysis, there was a significant publication bias based on Beggeru2019s test (p 0.0001). * Could the authors elaborate on this test? ,
Preconditioning with endoplasmic reticulum stress mitigates retinal endothelial inflammation via activation of X-box binding protein 1
Authors: Sarah X Zhang
Joshua J Wang
Jingming Li
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Endoplasmic reticulum stress; X-box binding protein 1; vascular inflammation; retinal adhesion molecule expression; leukostasis
Affiliations: Department of Medicine, Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Abstract:  Endoplasmic reticulum (ER) stress is widely implicated in various pathological conditions such as diabetes. Previously, we reported that enhanced ER stress contributes to inflammation and vascular damage in diabetic and ischemia-induced retinopathy. However, the exact role of the signaling pathways activated by ER stress in vascular inflammation remains poorly understood. In the present study, we investigated the role of X-box binding protein 1 (XBP1) in retinal adhesion molecule expression, leukostasis, and vascular leakage. Exposure of human retinal endothelial cells to low dose ER stress inducers resulted in a robust activation of XBP1 but did not affect inflammatory gene expression. However, ER stress preconditioning almost completely abolished TNF-α-elicited NF-κB activation and adhesion molecule ICAM-1 and VCAM-1 expression. Pharmaceutical inhibition of XBP1 activation or knockdown of XBP1 by siRNA markedly attenuated the effects of preconditioning on inflammation. Moreover, loss of XBP1 led to an increase in ICAM-1 and VCAM-1 expression. Conversely, overexpression of spliced XBP1 attenuated TNF-α-induced phosphorylation of IKK, IκBα, and NF-κB p65, accompanied by decreased NF-κB activity and reduced adhesion molecule expression. Finally, in vivo studies show that activation of XBP1 by ER stress preconditioning prevents TNF-α-induced ICAM-1 and VCAM-1 expression, leukostasis, and vascular leakage in mouse retinas. These results collectively indicate a protective effect of ER stress preconditioning against retinal endothelial inflammation, which is likely through activation of XBP1-mediated unfolded protein response (UPR) and inhibition of NF-κB activation. 

Retracted: No

PubPeer comments:
 In Fig.5C, there is a splice site (indicated with red box). Could author tell what happened ? ![file] ,
Manifestation of Y-chromosomal deletions in the human testis: a morphometrical and immunohistochemical evaluation
Authors: E Nieschlag
M Bergmann
M Simoni
S Von Eckardstein
M Engelhardt
C M Luetjens
J Gromoll
Journal: Human Reproduction (2002)
Discipline: CLINICAL MEDICINE
Keywords: AZF region; Y chromosome microdeletions; spermatogenesis; histological phenotypes; genetic analysis
Affiliations: Institute of Reproductive Medicine, Westphalian Wilhelms-University, Domagkstr. 11, D-48129 Muenster, Germany.

Abstract:  Background: Deletions of the AZF (azoospermia factor) subregions on the Y chromosome are accompanied by a diverse spectrum of spermatogenic disturbances ranging from hypospermatogenesis to total depletion of germ cells causing infertility. The AZF region encodes gene products which are candidates for the genetic control of spermatogenesis. Although it is known which genes are involved, a general principle of cause and effect cannot yet be deciphered and the deletion type has non-uniform histological phenotypes. Methods and results: We analysed morphological parameters of testicular biopsies from 17 patients diagnosed for Y chromosome microdeletions. As control groups we analysed testes from patients with idiopathic Sertoli cell-only (SCO) syndrome (n = 11), mixed atrophy (n = 10) and complete spermatogenesis (n = 11). A detailed genetic analysis on the extension of the observed microdeletions revealed similar breakpoints in the distal and proximal region of the AZFc region, indicating a common mechanism of homologous recombination for such deletions, as has been suggested before. Morphometric parameters such as the diameter of the tubules, lumen, thickness of the lamina propria and height of the tubule epithelia were investigated. The diameter of the tubules from patients with microdeletions was found to be significantly smaller compared with patients with mixed atrophy. Considering also the size of the tubules, lumen and epithelia, a Y-chromosomal microdeletion represents an intermediate state between an idiopathic SCO and normal spermatogenesis. The immunohistochemical analysis of six different Sertoli cell markers, cytokeratin 18, vimentin, inhibin alpha subunit, 14-3-3 theta, FSH receptor and androgen receptor, revealed no impact of AZF deletion on the specific expression pattern of these genes. Conclusions: Our results suggest that, notwithstanding the deletion of a common region in the AZFc region, microdeletions of the Y chromosome lead to an intermediate status between idiopathic SCO and complete spermatogenesis, resulting in a heterogeneous histological profile regardless of the seminiferous activity. The Sertoli cell function seems not to be altered. 

Retracted: No

PubPeer comments:
 Two Fig 2a images share many internal features but are not identical, including color. Scale bar suggests they are same magnification, but feature size appears to differ. Description suggests these are from different types of patients. Could the authors please comment? *** ![file] ,