PReD-Bench/PRed-Bench huggingface dataset:
MicroRNA-206 inhibits the viability and migration of medulloblastoma cells by targeting LIM and SH3 protein 1
Authors: Zhenwen Zheng
Xuexia Pan
Bin Wan
Zhimin Wang
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: LIM and SH3 protein 1; medulloblastoma; microRNA; migration; viability.
Affiliations: Third Department of Pediatrics, People's Hospital of Binzhou, Binzhou, Shandong 256610, P.R. China., Department of Hematology, People's Hospital of Binzhou, Binzhou, Shandong 256610, P.R. China., Department of Neonatology, Affiliated Hospital of Binzhou Medical College, Binzhou, Shandong 256603, P.R. China.

Abstract:  MicroRNA (miR)-206 has been found to be deregulated in various types of human cancer, including medulloblastoma. However, the regulatory mechanism of miR-206 in medulloblastoma growth and metastasis remains largely unclear. In the present study, reverse transcription-quantitative polymerase chain reaction data indicated that miR-206 was significantly downregulated in medulloblastoma tissues compared with adjacent non-tumor tissues (P&lt;0.01). Furthermore, low expression of miR-206 was significantly associated with seeding at presentation and anaplastic histology (P&lt;0.01), but not with sex, age, or residual tumors. Overexpression of miR-206 significantly reduced the viability and migration of medulloblastoma D341 cells (P&lt;0.01). LIM and SH3 protein 1 (LASP1) was further identified as a novel target of miR-206 in D341 cells. mRNA levels of LASP1 were significantly higher in medulloblastoma tissues compared to adjacent non-tumor tissues (P&lt;0.01), with an inverse correlation to the miR-206 levels in medulloblastoma tissues. In addition, protein expression levels of LASP1 ere negatively regulated by miR-206 in D341 cells. Further investigation showed that overexpression of LASP1 significantly eliminated the inhibitory effects of miR-206 on the migration and invasion of D341 cells (P&lt;0.01). In conclusion, our study demonstrates that miR-206 has a suppressive role in medulloblastoma cell viability and invasion, partly at least, via the targeting of LASP1. Our study highlights the importance of the miR-206/LASP1 in medulloblastoma. 

Retracted: No

PubPeer comments:
 *[above]* Figs 2C, 7C.  wound healing assay . *[below]* Fig 6C from [Wang et al (2017)] .  Wound healing . Rotated through 180 deg for ease of comparison.  How to explain the shared panel? ,
Hepatitis C Virus Core Protein Modulates Endoglin (CD105) Signaling Pathway for Liver Pathogenesis
Authors: Young-Chan Kwon
Keith Meyer
Reina Sasaki
Ranjit Ray
Journal: Journal of Virology (2017)
Discipline: MICROBIOLOGY
Keywords: HCC; HCV; angiogenesis; core; endoglin
Affiliations: Department of Internal Medicine, Saint Louis University, St. Louis, Missouri, USA., Department of Internal Medicine, Saint Louis University, St. Louis, Missouri, USA ., Department of Molecular Microbiology & Immunology, Saint Louis University, St. Louis, Missouri, USA.

Abstract:  Endoglin is part of the TGF-Œ≤ receptor complex and has a crucial role in fibrogenesis and angiogenesis. It is also an important protein for tumor growth, survival, and cancer cell metastasis. In a previous study, we have shown that hepatitis C virus (HCV) infection induces epithelial-mesenchymal transition (EMT) state and cancer stem-like cell (CSC) properties in human hepatocytes. Our array data suggested that endoglin (CD105) mRNA is significantly upregulated in HCV-associated CSCs. In this study, we have observed increased endoglin expression on the cell surface of an HCV core-expressing hepatocellular carcinoma (HepG2) cell line or immortalized human hepatocytes (IHH) and activation of its downstream signaling molecules. The status of phospho-SMAD1/5 and the expression of inhibitor of DNA binding protein 1 (ID1) were upregulated in HCV-infected cells or viral core gene-transfected cells. Additionally, we observed upregulation of endoglin/ID1 mRNA expression in chronic HCV patient liver biopsy samples. CSC generation by HCV core protein was dependent on the endoglin signaling pathway using activin receptor-like kinase 1 (ALK1) Fc blocking peptide and endoglin small interfering RNA (siRNA). Further, follow-up from in vitro analysis suggested that the antiapoptosis Bcl2 protein, proliferation-related cyclin D1 protein, and CSC-associated Hes1, Notch1, Nanog, and Sox2 proteins are enhanced during infection or ectopic expression of HCV core protein.IMPORTANCE Endoglin plays a crucial role in fibrogenesis and angiogenesis and is an important protein for tumor growth, survival, and cancer cell metastasis. Endoglin enhances ALK1-SMAD1/5 signaling in different cell types, leading to increased proliferation and migration responses. We have observed endoglin expression on the HCV core-expressing cell surface of human hepatocyte origin and activation of phospho-SMAD1/5 and ID1 downstream signaling molecules. ID1 protein plays a role in CSC properties, and we found that this pathway is important for antiapoptotic and cell proliferation signaling. Blocking of endoglin-ALK1-SMAD1/5 might be a good candidate for therapy for liver cancer stem cells together with liver cirrhosis. 

Retracted: No

PubPeer comments:
 Could the authors compare Figures 5C and 6A? It appears to my eye that this has been repeated, although the captions read differently (it appears to me that the mistake is with 6A). ***  , 
 #1 Let the journals know your concern. Thanks. , 
 #2 Do you agree that this is an error or am I mistaken? , 
 July 1, 2020  ,
Functional interaction between PML and SATB1 regulates chromatin-loop architecture and transcription of the MHC class I locus
Authors: Sanjeev Galande
Pavan P Kumar
Dimple Notani
Oliver Bischof
Prabhat Kumar Purbey
Henning Urlaub
Anne Dejean
Journal: Nature Cell Biology (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PML; higher-order chromatin organization; gene regulation; matrix attachment region (MAR); SATB1
Affiliations: National Centre for Cell Science, Ganeshkhind, Pune 411007, India.

Abstract:  The function of the subnuclear structure the promyelocytic leukaemia (PML) body is unclear largely because of the functional heterogeneity of its constituents. Here, we provide the evidence for a direct link between PML, higher-order chromatin organization and gene regulation. We show that PML physically and functionally interacts with the matrix attachment region (MAR)-binding protein, special AT-rich sequence binding protein 1 (SATB1) to organize the major histocompatibility complex (MHC) class I locus into distinct higher-order chromatin-loop structures. Interferon gamma (IFNgamma) treatment and silencing of either SATB1 or PML dynamically alter chromatin architecture, thus affecting the expression profile of a subset of MHC class I genes. Our studies identify PML and SATB1 as a regulatory complex that governs transcription by orchestrating dynamic chromatin-loop architecture. 

Retracted: No

PubPeer comments:
 Figure 5a. Much more similar than you would expect.  , 
 #1 I agree. I came across this independently. ***  , 
 I disagree, They look different.  , 
 #2 Hydraena Serricollis and Actinopolyspora Biskrensis, Before making any claims, one needs to have a careful look at the published pictures. I analyzed these two blots with available online tools that can analyze the content between two pics and turned out they are completely different. what I suggest you is that, download high quality image of the published picture, enlarge it and evaluate yourself whether these blots are same or different. , 
 #4 I appreciate your thoroughness and feedback. I agree that your analysis demonstrates more clearly the differences. Would you care to share what online tool you used? , 
 Figure S5 u2013 The Full scans of Western blots are showed. Contrast enhanced. The lanes contain splices, could authors check this issue, please?  , 
 #4 I adjusted the contrast of the IFNy-treated 105F-1aR band to more closely match the Control band and looked at the result using false color. I reiterate my earlier agreement with #1 that these bands appear very similar. Do the authors have the original data? ***  ,
Myeloid derived suppressor cells contribute to the malignant progression of oral squamous cell carcinoma
Authors: Hua-Yang Fan
Ke Wang
Ya-Ling Tang
Sha-Sha Wang
Xiang-Hua Yu
Xin Pang
Jing-Biao Wu
Ya-Jie Tang
Lu-Ling Dai
Hao-Fan Wang
Ming-Xin Cao
Xin-Hua Liang
Journal: PLoS ONE (2020)
Discipline: Multidisciplinary
Keywords: MDSCs; oral squamous cell carcinoma; crosstalk; tumor progression; immunosuppressive cells
Affiliations: State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China., State Key Laboratory of Microbial Technology, Shandong University, Qingdao, China.

Abstract:  Purpose: The tumor-related myeloid derived suppressor cells (MDSCs), important immunosuppressive cells in tumor microenvironment, play an important role in the cancer progression. This study is aimed to investigate the crosstalk between MDSCs and oral squamous cell carcinoma (OSCC) cells and their role in the malignant progression of OSCC. Methods: Immunochemistry (IHC) was used to investigate the expression of CD33 in 200 OSCC, 36 premalignant. CD33+ MDSCs were sorted and enriched via magnetic-activated cell sorting (MACS) from OSCC patients or health donor, and their phenotypes were identified by flow cytometry. With a co-culture system of MDSCs and OSCC, the effects of MDSCs on OSCC proliferation, apoptosis, migration invasion, epithelial-mesenchymal transition (EMT), and vasculogenic mimicry formation (VM) formation were assessed, respectively. Besides, peripheral blood mononuclear cells (PBMCs) from health donor were cultured with OSCC supernatant, the level of MDSCs and expressions of Arginase (Arg-1) and inducible nitric oxide synthase (iNOS) were measured. Results: The number of MDSCs was increased in tumor tissues of OSCC patients, and was positively related to the T stage, pathological grade, lymph node metastasis and poor prognosis. Tumor-related MDSCs of the co-culture system promoted OSCC progression by contributing to cell proliferation, migration and invasion as well as inducing EMT and VM. In turn, OSCC cells had potential to induce MDSCs differentiation from PBMCs and increase the expression of Arg-1 and iNOS. Conclusion: These indicated that the crosstalk between MDSCs and tumor cells facilitated the malignant progression of OSCC cells and the immune suppressive properties of MDSCs, which may provide new insights into tumor treatment on targeting tumor-associated immunosuppressive cells. 

Retracted: No

PubPeer comments:
 Figure 3A appears to have some images which overlap. ***  , 
 Figure 5A also. ***  , 
 Thanks for your information! We had carefully checked the figures and found that the images were different. , 
 #3 Thank you for your reply. As this is clearly not true, I will suggest the journal investigate. This lab appears to have more than a [dozen papers] with similar concerns. ,
Effect of lentiviral vector-mediated KSR1 gene silencing on the proliferation of renal tubular epithelial cells and expression of inflammatory factors in a rat model of ischemia/reperfusion injury
Authors: Guanghong Han
Lili Yu
Xiadong Du
Yang Bai
Kaimin Guo
Ying Xu
Journal: Acta Biochimica et Biophysica Sinica (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Renal ischemia/reperfusion; lentiviral vector; KSR1 gene silencing; inflammatory factors; proliferation
Affiliations: Department of Ultrasound, The First Hospital of Jilin University, Changchun, China., Department of Oral Geriatrics, School and Hospital of Stomatology, Jilin University, Changchun, China., Department of Andrology, The First Hospital of Jilin University, Changchun, China., Social Development Bureau, Changchun Jingyue High-Tech Industrial Development Zone Management Committee, Changchun, China., Department of Nephrology, The First Hospital of Jilin University, Changchun, China.

Abstract:  Renal ischemia/reperfusion (I/R) is a common cause of acute renal failure in many clinical settings. Our study aimed to elucidate the role of lentiviral vector-mediated KSR1 gene silencing in inflammatory factor expression and proliferation of renal tubular epithelial cells (RTECs) in a rat model of I/R injury. Male Sprague-Dawley (SD) rats were used for I/R model establishment and subject to different treatments, followed by the measurement of neurological severity score (NSS), tumor necrosis factor-Œ± (TNF-Œ±), interleukin (IL)-6, IL-1Œ≤, 47-kDa heat-shock protein (HSP47), KSR1, and factors related to the Ras/MAPK pathway, as well as cell apoptosis. As compared with the blank group, the neurologic impairment induced by I/R in the siKSR1, U0126, and siKSR1 + U0126 groups was alleviated. Compared with the control group, the other five groups showed increased levels of TNF-Œ±, IL-6, IL-1Œ≤, HSP47, N-ras, Raf-1, c-fos, TNF-Œ±, IL-6, p38 MAPK, and cell apoptosis, accompanied by a declined mRNA and protein level of Bcl-2. As compared with the blank and NC groups, the siKSR1, U0126, and siKSR1 + U0126 groups showed decreased levels of TNF-Œ±, IL-6, IL-1Œ≤, HSP47, N-ras, Raf-1, c-fos, TNF-Œ±, IL-6, p38 MAPK, cleaved caspase-3, cleaved caspase-9, p53, and cell apoptosis, accompanied by an increased mRNA and protein level of Bcl-2. Our findings demonstrated that KSR1 gene silencing might inhibit the expression of inflammatory factors in RTECs and promote their proliferation by inactivating the Ras/MAPK pathway in the rat model of I/R injury. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have some unexpected repetitive features. Could the authors check, please?  , 
 Figure 5. The Blank and NC panels appear to show an area of overlap, shown here with red boxes.  , 
 Figure 7. Traces of picture cropping.  ,
Nanostructured Lipid Carriers of Pioglitazone Loaded Collagen/Chitosan Composite Scaffold for Diabetic Wound Healing
Authors: Monica Gulati
Mehjabeen Bano
Bharat Kumar Reddy Sanapalli
Sachin Kumar Singh
Veera Venkata Satyanarayana Reddy Karri
Jawahar Natarajan
Journal: Advances in Wound Care (2019)
Discipline: CLINICAL MEDICINE
Keywords: chitosan; collagen; nanostructured lipid carrier; pioglitazone; scaffold and diabetic wound.
Affiliations: Department of Pharmaceutics, JSS College of Pharmacy, Ooty, JSS Academy of Higher Education and Research, India., Department of Pharmacology, JSS College of Pharmacy, Ooty, JSS Academy of Higher Education and Research, India., School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, India., Faculty of Applied Medical Sciences, Lovely Professional University, Phagwara, India.

Abstract:  Diabetic wound is a major problem that often needs amputation of the concerned organ in patients suffering from diabetes. In diabetes, the prolonged phase of inflammation obstructs the further phases of healing which, in turn, lead to improper healing of the wounds in diabetes. Pioglitazone (Pio) hydrochloride is an antidiabetic drug with reported anti-inflammatory properties. The aim of this study was to develop a Pio-nanostructured lipid carrier (Pio-NLC)-loaded collagen/chitosan (COL-CS) scaffold and evaluate its healing ability in diabetic wounds. The results of characterization of composite scaffolds reveal that cross-linked scaffolds possess optimum porosity, low matrix degradation, and sustained drug release compared with noncross-linked scaffolds. The in vitro studies reveal that the Pio-NLC-COL-CS scaffold was biocompatible and enhanced cell growth compared with control and NLC-COL-CS. Using the streptozotocin-induced diabetic wound model, significantly (p &lt; 0.001) higher rates of wound contraction in Pio-NLC-COL-CS scaffold-treated group were observed in comparison with that in control and NLC-COL-CS-treated group. The enzyme-linked immunosorbent assay results indicate a significant (p &lt; 0.001) decrease of matrix metalloproteinases-9 levels in the Pio-NLC-COL-CS-treated group compared with those in control group. Use of nanostructured lipid carrier (Pio-NLC-COL-CS) scaffold can prove to be a promising strategy for local treatment for diabetic wounds. 

Retracted: No

PubPeer comments:
 Figure 3. One of the panels in Figure 3A (NLC-COL-CS scaffold) looks very similar to a panel in Figure 3B (Pio-NLC-COL-CS scaffold). Shown with red boxes.  , 
 Figure 9: Two sets of panels share unexpected similarities. Day7 NLC-COL-CS appears to show an area of overlap with Day 14 NLC-COL-CS - shown with green boxes. Day21 Control appears to show an area of overlap with Day 21 NLC-COL-CS - shown with blue boxes.  ,
lncRNA HOTAIR promotes gastric cancer proliferation and metastasis via targeting miR-126 to active CXCR4 and RhoA signaling pathway
Authors: Fu-Sheng Gong
Hao Lai
Sheng-Hong Wei
Jun Xiao
Zai-Sheng Ye
Lu-Chuan Chen
Journal: Cancer Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: HOTAIR; CXCR4; RhoA; gastric cancer; metastasis
Affiliations: Department of Gastrointestinal Surgery, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou, 350001, China., Department of Gastrointestinal Surgery, Guangxi Cancer Hospital, Guangxi Medical University Cancer Hospital, Nanning, 530001, China., Department of Molecular immune laboratory, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou, 350001, China.

Abstract:  HOTAIR, a well-known long noncoding RNAs (lncRNA), has been recognized to contribute to the tumor metastasis in several tumors. But its role in gastric cancer remains elusive. Here, we reported an increase in HOTAIR promoted proliferation and metastasis of gastric cancer cell lines. The HOTAIR and miR-126 level was determined in 15 paired primary gastric cancer tissues and their adjacent noncancerous gastric tissues. Over-expression or downregulation HOTAIR was conducted in AGS or BGC-823 cells to investigate the impact of HOTAIR in proliferation and metastasis. Then dual luciferase reporter assay was utilized to study the interaction between CXCR4 and miR-126. Cells transfected with shHOTAIR or miR-126 mimic were subjected to western blot to investigate the role of SDF-1/CXCR4 signaling in HOTAIR mediated proliferation and metastasis. HOTAIR was highly expressed in gastric cancer tissues and several gastric cancer cell lines. Overexpressed HOTAIR facilitated proliferation and metastasis in vitro while HOTAIR knockdown inhibit proliferation and metastasis. A negative correlation was observed between miR-126 and HOTAIR. And, we also confirmed the decrease in miR-126 in clinic specimen. Furthermore, HOTAIR and miR-126 negatively regulated each other and then increase or decrease CXCR4 expression and downstream pathway, respectively. CXCR4 was confirmed as a direct target of miR-126. Our study demonstrated that high HOTAIR expression promote proliferation and metastasis in gastric cancer via miR-126/CXCR4 axis and downstream signaling pathways. 

Retracted: No

PubPeer comments:
 Figs 3B, 5C, 5F.  I urge the authors to check their choice of illustrations. , 
 Corrected [22 November 2021] . ----------------------- In the article by Xiao et al.,1 entitled u201clncRNA HOTAIR promotes gastric cancer proliferation and metastasis via targeting miR-126 to active CXCR4 and RhoA signaling pathway,u201d the author wants to correct figure parts 2D, 3D, 5C, and 5F. Corrected Figure 2D.  Corrected Figure 3D.  Corrected Figure 5C.  Corrected Figure 5F.  , 
 The correction did not affect *[left]* Figs 3C and 5E, here compared with *[right]* Fig 2B from  Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt u03b2-catenin signaling pathway in bladder cancer ([Hu et al 2017] ).  ,
Retraction: MicroRNA-451 blockade promotes osteoblastic differentiation and skeletal anabolic effects by promoting YWHAZ-mediated RUNX2 protein stabilization
Authors: Katie Lim
Journal: RSC Medicinal Chemistry (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Retraction; Article; DOI; Research; Abstract
Affiliations: Royal Society of Chemistry, Thomas Graham House, Cambridge, UK

Abstract:  [This retracts the article DOI: 10.1039/C8MD00187A.]. 

Retracted: No

PubPeer comments:
 Retracted [15 January 2021] : ----------------------------------------- The Royal Society of Chemistry hereby wholly retracts this MedChemComm article due to concerns with the reliability of the data. The images in the article, and the raw data provided by the authors, were screened by an image integrity expert. The images of the cultures in Fig. 2, 3 and 5 show signs of cloning as duplicating features can be observed, which indicates that the images have been manipulated. In addition, the raw data provided for the Western blot images does not appear to be genuine. In most of the raw images, the area immediately around the bands has a different structure or appearance to the surrounding area. Furthermore, there are traces of cloning in the background of the raw data for multiple panels including Fig. 3C (AKT), Fig. 3C (SMURF2) and Fig. 3J (p-AKT), indicating that the raw data was manipulated. Therefore, the raw data provided by the authors cannot be used to validate the published data. Given the significance of the concerns about the validity of both the data in the article and the raw data provided by the authors, the findings presented in this paper are not reliable. The authors have been informed but have not responded to any correspondence regarding the retraction. -------------------------------------------------------- Here highlighting FIg 4B,  Representative micro-CT images of the femoral epiphyses in sham and OVX mice -- not mentioned in the retraction.  It is not often you see signs of a Photoshop origin in what are computer-synesthised images already.  , 
 *The images of the cultures in Fig. 2, 3 and 5 show signs of cloning as duplicating features can be observed* Fig 5(C).  Representative images of alizarin-positive colony formation .  ,
Transcriptional regulation of urokinase (uPA) gene expression in breast cancer cells: role of DNA methylation
Authors: S A Rabbani
R H Xing
Journal: International Journal of Cancer (1999)
Discipline: CLINICAL MEDICINE
Keywords: breast carcinoma; hormone sensitivity; urokinase (uPA); DNA methylation; transcriptional suppression
Affiliations: Department of Medicine, McGill University, Montreal, QC, Canada.

Abstract:  Carcinoma of the breast is a leading hormone-dependent malignancy, resulting in a high rate of morbidity and mortality. During the complex multi-step process of tumor promotion, this common cancer is initiated as hormone-responsive (HR), non-metastatic cancer, followed by a gradual transition into a highly metastatic hormone-insensitive (HI) variety which lacks the functional estrogen receptor. This transition of cancer cells causes them to become refractory to hormonal treatment. Urokinase (uPA), a member of the serine protease family has been implicated in the progression of several malignancies including breast cancer. In the current study, we have examined the correlation between hormone sensitivity and uPA expression in HR normal mammary epithelial cells (HMEC) and in MCF-7 and T-47D breast cancer cell lines. Comparison was made with HI breast cancer cells MDA-231. uPA mRNA expression was seen only in the highly invasive, HI breast cancer cells MDA-231. Lack of uPA expression in HR normal (HMEC) and in minimally invasive, HR cells (MCF-7 and T-47D) was due to transcriptional suppression of uPA gene expression as determined by nuclear run-off assays. Since alteration of the DNA methylation status of CpG island in the 5' sequence of oncogenes and tumor suppressor genes has been demonstrated to change their expression, we examined DNA methylation as a potential molecular mechanism for regulating uPA gene transcription in these cancer cells. Southern blot analysis using methylation sensitive enzymes revealed that CpG island of uPA gene are methylated in HR, HMEC, MCF-7 and T-47D cells, whereas they are hypomethylated in HI and MDA-231 cells. Treatment of HR MCF-7 cells with cytosine DNA methyltransferase inhibitor 5' azacytidine caused a dose-dependent induction of uPA mRNA due to demethylation of the CpG island of the uPA gene which led to increased invasive ability of these HR cancer cells. Our results demonstrate that DNA methylation can regulate the transcription of the uPA gene to alter the invasive behaviour of these HR breast cancer cells. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected.  ,
Tonifying spleen and replenishing kidney method of traditional Chinese medicine for myasthenia gravis: A protocol for systematic review and meta-analysis
Authors: Jiachun Lu
Xueping Yang
Min He
Lu Li
Weiyin Chen
Yuxuan Peng
Bibo Lu
Qing Ye
Yuting Pan
Journal: Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: Myasthenia gravis; autoimmune disorder; traditional Chinese medicine; tonifying the spleen; replenishing the kidney
Affiliations: Chengdu Eighth People's Hospital (Geriatric Hospital of Chengdu Medical College)., Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Abstract:  Background: Myasthenia gravis (MG) is an autoimmune antibody-mediated disorder caused by dysfunction at the neuromuscular junction spreads. The main clinical features of this disease are fluctuating fatigue, and weakness of the skeletal muscles of the eyes and limbs. At present, the tonifying the spleen and replenishing the kidney method in traditional Chinese medicine has been widely used for MG. The present study was conducted to evaluate the efficacy and safety of the tonifying the spleen and replenishing the kidney method in traditional Chinese medicine for MG. Methods: The following 10 databases were searched from inception to March 2021: PubMed, Cochrane Library, EMBASE, Web of Science, Springer, China National Knowledge Infrastructure (CNKI), Wan fang, VIP Chinese Science and Technique Journals Database, the Chinese Bio Medical Database (CBM), and Baidu Scholar. The language was limited to the Chinese and English language. Merely randomized controlled trials (RCTs) were included. The Cochrane Collaboration risk-of-bias tool was used for the methodological quality assessment and risk of bias. The meta-analysis was assessed using the Cochrane RevMan 5.3 software. Results: In the present study, a meta-analysis was conducted, and RCTs that met the eligibility criteria were included. Furthermore, the different outcome indicators of different methods were objectively compared. The main outcome indicators included the effective rate, quantitative myasthenia gravis (QMG) scores, adverse events, and quality of life (QOL). The secondary outcome indicators included AchRAb, serum-related immune cells (such as CD3+CD4+cells and CD4+/CD8+cells), the traditional Chinese medicine syndrome score scale (TCMSSS), the serum interleukin-6 level, the level of IFN-Œ≥ and its mRNA, and the clinical score that contains the clinical absolute score (CAS) and clinical relative score (CRS). Conclusion: This study would provide credible evidence to determine whether the tonifying the spleen and replenishing the kidney method in traditional Chinese medicine is an effective treatment method for MG. Trial registration number: INPLASY202110097. 

Retracted: No

PubPeer comments:
 This paper makes frequent reference to the  the tonifying the spleen and replenishing the kidney method in TCM but fails to define what that is for the reader ,
Interferon alpha-2b inhibits negative-strand RNA and protein expression from full-length HCV1a infectious clone
Authors: Ramesh Prabhu
Virendra Joshi
Salima Haque
Frank Bastian
Fredric Regenstein
Robert F Garry
Srikanta Dash
Swan Thung
Journal: Experimental and Molecular Pathology (2004)
Discipline: CLINICAL MEDICINE
Keywords: T7-based model system; hepatitis C virus (HCV); replication-defective adenovirus; T7 RNA polymerase; HCV cDNA clone
Affiliations: Department of Pathology and Laboratory Medicine, Tulane University Health Science Center, New Orleans, LA 70112, USA.

Abstract:  We have established a T7-based model system for hepatitis C virus (HCV) 1a strain, which involves the use of a replication-defective adenovirus that carries the gene for T7 RNA polymerase and a transcription plasmid containing full-length HCV cDNA clone. To facilitate high-level expression of HCV, sub-confluent Huh7 cells were first infected with adenovirus containing the gene for the T7 RNA polymerase and then transfected with the transcription plasmid. As a negative control, part of NS5B gene of this clone was deleted which abolishes the HCV RNA-dependent RNA polymerase and prevents replication of viral RNA. This model produces high levels of structural (core, E1, E2) and nonstructural proteins (NS5), which were detected by Western blot analysis and immunofluorescence assay. Negative-strand HCV RNA was detected only in the wild-type clone in the presence of actinomycin D, and no RNA was detected with the NS5B deleted mutant control. As a practical validation of this model, we showed that IFN alpha-2b selectively inhibits negative-strand RNA synthesis by blocking at the level of protein translation. The inhibitory effect of IFN alpha-2b is not due reduction of transcription by T7 polymerase or due to intracellular degradation of HCV RNA. This in vitro model provides an efficient and reliable means of assaying negative-strand RNA, protein processing, and testing the antiviral properties of interferon. 

Retracted: No

PubPeer comments:
 Figure 7A. Some panels here appear to show an overlap with panels in Figure 9 of another paper by some of the same authors, i.e. Srikanta Dash et al., Liver International (2005), DOI: 10.1111 j.1478-3231.2005.01082.x - https: pubpeer.com publications 77469D9D0734908B980923D3C4DF66 Here is a comparison of the two figures, with similar looking areas marked with boxes of the same color.   , 
 Figure 5. * Orange boxes: In the top part of the figure, the left panels look very similar. Would that be expected? * Green boxes: In the bottom part of the figure, the left panels look very similar. Would that be expected?  Also, Figure 5 looks remarkably similar to Figure 10 in another paper by the same research group, i.e. Ramesh Prabhu et al., American Journal of Pathology (2004), DOI: 10.1016 S0002-9440(10)63377-9 - https: pubpeer.com publications 424DFAE426D4B2A70FA7971E55A11F  , 
 Figure 6. * Blue boxes: The right two panels in 6B look very similar to each other.  ,
Lipase maturation factor LMF1, membrane topology and interaction with lipase proteins in the endoplasmic reticulum
Authors: Ciara M Gallagher
Maryam Hosseini
Osnat Ben-Zeev
Jo Ling-Liao
Mark H Doolittle
Mikl√≥s P√©terfy
Peter Walter
Fen Yin
Saskia B Neher
Howard Wong
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Lipase maturation factor 1; LMF1; endoplasmic reticulum; ER membrane; enzyme activity
Affiliations: Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. 

Abstract:  Lipase maturation factor 1 (LMF1) is predicted to be a polytopic protein localized to the endoplasmic reticulum (ER) membrane. It functions in the post-translational attainment of enzyme activity for both lipoprotein lipase and hepatic lipase. By using transmembrane prediction methods in mouse and human orthologs, models of LMF1 topology were constructed and tested experimentally. Employing a tagging strategy that used insertion of ectopic glycan attachment sites and terminal fusions of green fluorescent protein, we established a five-transmembrane model, thus dividing LMF1 into six domains. Three domains were found to face the cytoplasm (the amino-terminal domain and loops B and D), and the other half was oriented to the ER lumen (loops A and C and the carboxyl-terminal domain). This representative model shows the arrangement of an evolutionarily conserved domain within LMF1 (DUF1222) that is essential to lipase maturation. DUF1222 comprises four of the six domains, with the two largest ones facing the ER lumen. We showed for the first time, using several naturally occurring variants featuring DUF1222 truncations, that Lmf1 interacts physically with lipoprotein lipase and hepatic lipase and localizes the lipase interaction site to loop C within DUF1222. We discuss the implication of our results with regard to lipase maturation and DUF1222 domain structure. 

Retracted: Yes

PubPeer comments:
 Withdrawal: Lipase maturation factor LMF1, membrane topology and interaction with lipase proteins in the endoplasmic reticulum. VOLUME 284 (2009) PAGES 33623u201333633 This article has been withdrawn by Mark H. Doolittle, Saskia B. Neher, Osnat Ben-Zeev, Ciara M. Gallagher, Maryam Hosseini, Peter Walter, and Miklu00f3s Pu00e9terfy. Jo Ling-liao, Fen Yin and Howard Wong have not responded. After a review of the data, one of the corresponding authors (M. P.) learned that there was duplication and inappropriate manipulation of images in Fig. 7, raising concerns about the validity of the conclusions drawn from the results. The Walter laboratory (S. B. N., C. M. G., and P. W.) was not involved in the generation, presentation, or interpretation of the data in Fig. 7. u00a9 2019 by The American Society for Biochemistry and Molecular Biology, Inc. , 
 Figure 7. ***  ,
Asymmetrically twisted phenanthrimidazole derivatives as host materials for blue fluorescent, green and red phosphorescent OLEDs
Authors: Sekar Panimozhi
Jayaraman Jayabharathi
Venugopal Thanikachalam
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: electroluminescent properties; twisted phenanthrimidazole derivatives; blue OLEDs; deep-blue emission; pyrene
Affiliations: Department of Chemistry, Annamalai University, Annamalai nagar, 608 002, Tamilnadu, India. ., Department of Chemistry, Annamalai University, Annamalai nagar, 608 002, Tamilnadu, India.

Abstract:  The electroluminescent properties of asymmetrically twisted phenanthrimidazole derivatives comprised of fluorescent anthracene or pyrene unit namely, 1-(1-(anthracen-10-yl)naphthalen-4-yl)-2-styryl-1H-phenanthro[9,10-d]imidazole (ANSPI), 1-(1-(pyren-1-yl) naphthalene-4-yl)-2-styryl-1H-phenanthro[9,10-d]imidazole (PNSPI), 4-(2-(4-(anthracen-9-yl) styryl)-1H-phenanthro[9,10-d]imidazol-1-yl)naphthalene-1-carbonitrile (ASPINC) and 4-(2-(4-(pyren-1-yl)styryl)-1H-phenanthro[9,10-d]imidazol-1-yl)naphthalene-1-carbonitrile (PSPINC) for blue OLEDs have been analyzed. The asymmetrically twisted conformation interrupt œÄ-conjugation effectively results in deep-blue emission. The pyrene containing PSPINC based non-doped blue device (476 nm) shows maximium efficiencies (current efficiency (Œ∑c)-4.23 cd/A; power efficiency (Œ∑p)-2.86 lm/W; external quantum efficiency (Œ∑ex)-3.48%: CIE (0.16, 0.17) at 3.10 V. Among the doped blue devices, An(PPI)2:ASPINC shows high efficiencies (Œ∑c-12.13 cd/A; Œ∑p-5.98 lm/W; Œ∑ex-6.79%; L-23986 cd m-2; EL-458 nm) at 3.15 V with CIE (0.15, 0.17) than An(PPI)2:PSPINC based device which is inconsistent with non-doped device performances. The green and red PhOLEDs show higher efficiencies with Ir(ppy)3: ASPINC (Œ∑c-50.6 cd/A; Œ∑p-53.4 lm/W; Œ∑ex-17.0%; L-61581 cd m-2; EL-501 nm, CIE (0.31, 0.60) at 3.32 V and (bt)2Ir(dipba): ASPINC (Œ∑c-15.2 cd/A; Œ∑p-16.5 lm/W; Œ∑ex-14.5%; L-13456 cd m-2; EL-610 nm), CIE (0.63, 0.36) at 3.20 V, respectively. The complete energy transfer between the host and dopant molecules improved the efficiency of PHOLEDs. 

Retracted: No

PubPeer comments:
 Figure 3D: AFM images of ANSPI, PNSPI, ASPINC and PSPINC. Here is the figure as provided in the paper:  * The ANSPI and ASPINC panels share lots of similar areas if one of the two panels is rotated and mirrored. * The PNSPI and PSPIN panels share lots of similar areas if one of the two panels is rotated and mirrored. * Some areas might be visible multiple times within the same panel * Although the background areas look similar, the position of the white dots appears to vary  ,
How swamped preprint servers are blocking bad coronavirus research
Authors: Diana Kwon
Journal: Nature (2020)
Discipline: Multidisciplinary
Keywords: Publishing; SARS-CoV-2.

Abstract: Repositories are rapidly disseminating crucial pandemic science ‚Ä?and they‚Äôre screening more closely to guard against poor-quality work. Repositories are rapidly disseminating crucial pandemic science ‚Ä?and they‚Äôre screening more closely to guard against poor-quality work.

Retracted: No

PubPeer comments:
 The html version of this paper has the following title:  How swamped preprint servers are blocking bad coronavirus research https: www.nature.com articles d41586-020-01394-6 But the PDF version is:  How preprint servers are blocking bad coronavirus research https: media.nature.com original magazine-assets d41586-020-01394-6 d41586-020-01394-6.pdf It is unclear which is the  original title, or when the title was changed. Under  normal circumstances, a change in the title is accompanied by an author correction, erratum, or corrigendum, with its own independent DOI. But not here. There is no email indicated for the author, so how does one contact her for clarification? , 
 = http: www.dianakwon.com , 
 This is a news article, not a journal article. For magazine news and features, titles that appear in print are often shorter (and sometimes significantly different) from those that appear online. This is due to the fact that there s simply less space in print then there is on the web. Journalists would only issue an errata if there was an error in the title (either in print or online) that needed to be corrected. I believe different rules apply for journal articles. Cheers, Diana ,
Crocin protects against dexamethasone‚Äëinduced osteoblast apoptosis by inhibiting the ROS/Ca2+‚Äëmediated mitochondrial pathway
Authors: Hao Peng
Zhigang Nie
Shuang Deng
Lei Zhang
Qiang Lu
Sen Chen
Journal: Molecular medicine reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: Osteoblast apoptosis; glucocorticoid-induced osteoporosis; crocin; dexamethasone-induced apoptosis; MC3T3-E1 osteoblasts
Affiliations: Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Abstract:  Osteoblast apoptosis has been identified as an important event in the development of glucocorticoid (GC)‚Äëinduced osteoporosis and osteonecrosis of the femoral head. Crocin, a bioactive ingredient of saffron, has been demonstrated to induce antiapoptotic effects on numerous types of cell in vitro; however, the effects of crocin on the dexamethasone (Dex)‚Äëinduced apoptosis of osteoblasts remain unclear. In the present study, the protective effects of crocin during Dex‚Äëinduced apoptosis of MC3T3‚ÄëE1 osteoblasts, and the underlying mechanisms, were investigated. MTT and Annexin V‚ÄëFITC/PI flow cytometry assays were performed to evaluate the viability and apoptosis of cells, respectively. The mitochondrial transmembrane potential, reactive oxygen species (ROS), intracellular Ca2+ levels and apoptosis‚Äëassociated protein expression were assessed via flow cytometry, fluorescence microscopy and western blotting. It was demonstrated that crocin pretreatment inhibited Dex‚Äëinduced apoptosis of osteoblasts in a dose‚Äëdependent manner. Crocin reversed Dex‚Äëinduced decreases in the mitochondrial transmembrane potential, and increases in ROS and intracellular Ca2+ levels. Furthermore, crocin upregulated the expression levels of B‚Äëcell lymphoma-2 (Bcl‚Ä?) and mitochondrial cytochrome c (Cyt C), and downregulated those of cleaved caspase‚Ä?, cleaved caspase‚Ä?, Bcl‚Ä?‚Äëassociated X protein and cytoplasmic Cyt C. N‚Äëacetylcysteine, a ROS inhibitor, and 1,2‚Äëbis(2‚Äëaminophenoxy)ethane‚ÄëN,N,N',N'‚Äëtetraacetic acid, a calcium chelator, attenuated Dex‚Äëinduced osteoblast apoptosis, whereas H2O2 and ionomycin, a calcium ionophore that increases intracellular calcium levels, reversed the antiapoptotic effects of crocin on Dex‚Äëtreated osteoblasts. These results indicated that crocin may protect osteoblasts from Dex‚Äëinduced apoptosis by inhibiting the ROS/Ca2+‚Äëmediated mitochondrial pathway, thus suggesting that crocin has potential value as a treatment for GC‚Äëinduced bone diseases. 

Retracted: No

PubPeer comments:
 Figure 2A. * Blue boxes: The Crtr and Dex + Cro 5 uM panels appear to share a very similar lower left quadrant, as well as part of the upper left quadrant. Other parts of the panels look different.  ,
Long non-coding RNA CCAT1 promotes glioma cell proliferation via inhibiting microRNA-410
Authors: Xia-Qing Guo
Guo-Fei Li
Jian-Lei Zhang
Qi-Shun Zhang
Yan-Li Duan
Zhao-Hui Wang
Dong-Lin Zheng
Journal: Biochemical and biophysical research communications (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glioma; LncRNA-CCAT1; MiR-410; U251¬†cell.
Affiliations: Department of Internal Neurology, Huaihe Hospital of Henan University, Kaifeng 475000, China. Electronic address: ., Department of Internal Neurology, Huaihe Hospital of Henan University, Kaifeng 475000, China., Department of Ultrasound, Kaifeng Maternity Hospital, Kaifeng 475000, China.

Abstract:  Background and aim: Long non-coding RNAs have been confirmed to play a critical role in various cancers. In the present study, the effect of long non-coding RNA (lncRNA) CCAT1 on glioma cell proliferation and its potential mechanism were investigated. Methods and results: Real-time PCR results showed that lncRNA-CCAT1 expression was significantly upregulated in glioma cancer tissues and cell lines compared with controls. After inhibiting CCAT1 expression in glioma cell line U251 with siRNA-CCAT1 (si-CCAT1), the cell viability and cell colony formation were decreased, the cell cycle was arrested in G1 phase, and the cell apoptosis was increased. As reported in bioinformatics software starbase2.0, a total of 22 microRNAs were potentially targeted by CCAT1. It was confirmed that miR-410 was altered most by si-CCAT1. After up-regulating CCAT1 expression in U251 cells, miR-410 level was decreased. Luciferase reporter assay confirmed that CCAT1 targeted miR-410. Correlation analysis showed that CCAT1 expression was negatively related to miR-410 expression in glioma cancer tissues. In addition, down-regulation of miR-410 reversed the inhibitory effect of si-CCAT1 on glioma proliferation. Conclusion: These data demonstrated that lncRNA-CCAT1 promoted glioma cell proliferation via inhibiting miR-410, providing a new insight about the pathogenesis of glioma proliferation. 

Retracted: No

PubPeer comments:
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 Fig 2F:  Figure2. The effect of si-CCAT1 on U251 cell. ... Apoptosis. The comparison appears to be between si-NC and si-CCAT1 cultures. It is difficult to find cells in the left-hand panel that are not also present in the RH.  Here, the si-NC panel reversed and superimposed on the si-CCAT1 panel so that white and black dots are unique to the former and latter, while cells in common cancel out. Most of the si-NC points cancel out.  , 
 Figure 4F.  Anti-miR-410 reverse the effect of si-CCAT1 in U251 cell ... cell apoptosis. The cell were transfected with NC, si-CCAT1 and anti-miR-410, respectively.  Points in the left-hand panel are a subset of those in the central panel, i.e. the data plotted as  NC and  si-CCAT1 are from the same experiment. When the NC panel is reversed and superimposed on si-CCAT1, the NC points all cancel out and only black dots (cells unique to si-CCAT1) are visible.  For comparison, here s the RH panel (anti-miR-410) superimposed on si-CCAT1. The data sets are different enough that both white and black are visible.  ,
Use of flow cytometry to monitor Legionella viability
Authors: Fran√ßoise Berger
Bruno Pozzetto
Florence Grattard
Serge Riffard
S√©verine Allegra
Philippe Berthelot
Journal: Applied and Environmental Microbiology (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Legionella; viability; heat shock treatment; flow cytometric assay; FCA
Affiliations: Groupe Immunit√© des Muqueuses et Agents Pathog√®nes, EA3064, Facult√© de M√©decine J. Lisfranc, Universit√© Jean Monnet, Saint-Etienne, France.

Abstract:  Legionella viability was monitored during heat shock treatment at 70 degrees C by a flow cytometric assay (FCA). After 30 min of treatment, for 6 of the 12 strains tested, the FCA still detected 10 to 25% of cells that were viable but nonculturable (VBNC). These VBNC cells were able to produce ATP and to be resuscitated after culture on amoebae. 

Retracted: No

PubPeer comments:
 Figure 2. Three of the colony plates appear to look identical. Marked with red boxes.  ,
Flunarizine induces Nrf2-mediated transcriptional activation of heme oxygenase-1 in protection of auditory cells from cisplatin
Authors: Y-H Kim
K-S Kim
S-Y Park
K-M Lee
H-T Chung
S-Y Chung
H-S So
H-J Kim
S-K Moon
W-C Jang
C Park
J-K Kim
R-K Park
J-H Lee
Journal: Cell death and differentiation (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: cytoprotective mechanisms; flunarizine; cisplatin-induced death; auditory cells; Nrf2/Keap1
Affiliations: Vestibulocochlear Research Center & Department of Microbiology, Wonkwang University School of Medicine, Jeonbuk 570-749, Korea.

Abstract:  We investigated the cytoprotective mechanisms of flunarizine in cisplatin-induced death of auditory cells. Concomitant with an increase in viability, treatment with flunarizine resulted in a marked dissociation of Nrf2/Keap1 and subsequent intranuclear translocation of Nrf2, which was mediated by PI3K-Akt signaling. Overexpression of Nrf2 protected cells from cisplatin along with transcriptional activation of ARE to generate heme oxygenase-1 (HO-1). Pretreatment with flunarizine predominantly increased the transcriptional activity of HO-1 among Nrf2-driven transcripts, including HO-1, NQO1, GCLC, GCLM, GST micro-1, and GSTA4. Furthermore, both pharmacological inhibition and siRNA transfection of HO-1 completely abolished the flunarizine-mediated protection of HEI-OC1 cells and the primary rat (P2) organ of Corti explants from cisplatin. These results suggest that Nrf2-driven transcriptional activation of ARE through PI3K-Akt signaling augments the generation of HO-1, which may be a critically important determinant in cellular response toward cisplatin and the cytoprotective effect of flunarizine against cisplatin. 

Retracted: No

PubPeer comments:
 Figure 3d. Much more similar than expected. https: imgur.com 7QbG8rJ ,