PReD-Bench/PRed-Bench huggingface dataset:
Jawbone microenvironment promotes periodontium regeneration by regulating the function of periodontal ligament stem cells
Authors: Wenjia Liu
Bin Zhu
Xicong Zhao
Zhuojing Luo
Yan Jin
Yihan Liu
Hao Zhang
Journal: Scientific reports (2017)
Discipline: Multidisciplinary
Keywords: Tooth development; Jawbone; Mesenchymal stem cells; Periodontium; Dental germ
Affiliations: State Key Laboratory of Military Stomatology, Centre for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China., Department of Orthopedics Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China., Department of Stomatology, PLA Xizang Military Region General Hospital, Lhasa, Tibet, People's Republic of China., Department of Stomatology, PLA 301th Hospital, Beijing, People's Republic of China.

Abstract:  During tooth development, the jawbone interacts with dental germ and provides the development microenvironment. Jawbone-derived mesenchymal stem cells (JBMSCs) maintain this microenvironment for root and periodontium development. However, the effect of the jawbone microenvironment on periodontium tissue regeneration is largely elusive. Our previous study showed that cell aggregates (CAs) of bone marrow mesenchymal stem cells promoted periodontium regeneration on the treated dentin scaffold. Here, we found that JBMSCs enhanced not only the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) but also their adhesion to titanium (Ti) material surface. Importantly, the compound CAs of PDLSCs and JBMSCs regenerated periodontal ligament-like fibers and mineralized matrix on the Ti scaffold surface, both in nude mice ectopic and minipig orthotopic transplantations. Our data revealed that an effective regenerative microenvironment, reconstructed by JBMSCs, promoted periodontium regeneration by regulating PDLSCs function on the Ti material. 

Retracted: No

PubPeer comments:
 this paper suffers from measurement and modeling that should have precluded its publication. Voigt and Kou0308nigsberger have written an excellent post-publication comment: Comment on u201cStudy on Phase Equilibrium of the K+, Mg2+ Clu2212, SO42u2212 + H2O Quaternary System at 353.15 K and Its Applicationu201d https: dx.doi.org 10.1021 acs.jced.0c00397 J. Chem. Eng. Data I have entered a PubPeer entry to that comment Kang et al wrote a response that does not adequately address the criticisms. https: dx.doi.org 10.1021 acs.jced.0c00536 ,
RETRACTED ARTICLE: Down-regulated MicroRNA 148b expression as predictive biomarker and its prognostic significance associated with clinicopathological features in non-small-cell lung cancer patients
Authors: Emad Yahaghi
Naeemeh Ghasemkhani
Sahar Shadvar
Ebrahim Shakiba
Amir Jouya Talaei
Yasamin Masoudi
Peyman Karimi Goudarzi
Journal: Diagnostic Pathology (2015)
Discipline: CLINICAL MEDICINE
Keywords: Lung cancer; non-small cell lung cancer (NSCLC); miR-148b; biomarker; clinicopathological features
Affiliations: Brain and Spinal Injury Research Center, Neuroscience institute, Tehran University of Medical Science, Tehran, Iran., Department of Biophysics, Faculty of Life Science, Azad University of Varamin Pishva Branch, Varamin, Iran., Department of Genetics, Faculty of Life Science, Azad University of Tehran Medical Sciences Branch, Tehran, Iran., Department of Molecular Biology, Baqiyatallah University of Medical Sciences, Tehran, Iran., Department of Neurosurgery, AJA University of Medical Sciences, Tehran, Iran. ., Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Abstract:  Background: Lung cancer is most common and is the leading cause of cancer-related death in both men and women worldwide. Understanding of the molecular mechanisms underlying non-small cell lung cancer (NSCLC) development and progression are important. In the present study, we investigated the potential role of miR-148b expression analysis as potential lung cancer biomarker with the correlation of circulating miR-148b to clinicopathological features. Methods: A total of 104 NSCLC patients were diagnosed and cancer tissues together with adjacent normal tissues were evaluated. Quantitative Real-time PCR method was utilized to evaluate the expression levels of miR-148b. In addition, we investigated to clarify the relationship of miR-148b with clinicopathological features and survival in patients with NSCLC. Results: Our findings showed that miR-148b was downregulated in tumor tissues when compared with corresponding adjacent normal lung tissues (0.34 ± 0.13 vs. 1.00 ± 0.57, P &lt; 0.05). Moreover decreased expression of miR-148b was significantly related to TNM stage (P = 0.001) and lymph node-metastasis (P = 0.023). This findings suggested that miR-148b was down-regulated in NSCLC patients and may play a key role as a tumor suppressor gene in NSCLC. Kaplan-Meier survival analysis and log-rank test suggested that low-expression group of patients had significantly shorter overall survival than high-expression group (log-rank test: P = 0.031). Multivariate Cox proportional hazards model analysis indicated that low miR-148b expression was independently linked to poor survival of patients with NSCLC (HR = 3.215, 95 % CI: 1.543-10.621, P = 0.021) and other factors were not significant independent predictor of survival in patients with NSCLC. Conclusion: Our findings demonstrated that miR-148b may play a role as independent prognostic factor for patients with NSCLC. 

Retracted: Yes

PubPeer comments:
 Translation is available at: https: www.mv.helsinki.fi home hemila T3.pdf ,
Down-regulation of long non-coding RNA AFAP1-AS1 inhibits tumor growth, promotes apoptosis and decreases metastasis in thyroid cancer
Authors: Wencheng Dai
Bin Jiang
Ye Tian
Weixian Chen
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AFAP1-AS1; Apoptosis; Cell growth; Migration; Thyroid cancer.
Affiliations: Department of Radiotherapy & Oncology, The Second Affiliated Hospital of Soochow University, 215004, China; Department of Head and Neck Surgery, Nantong Tumor Hospital, 226361, China., Department of Radiotherapy & Oncology, The Second Affiliated Hospital of Soochow University, 215004, China. Electronic address: ., Department of Head and Neck Surgery, Nantong Tumor Hospital, 226361, China.

Abstract:  Long non-coding RNAs (lncRNAs), a new type of transcripts, play important roles in various cellular biological processes, involving tumorigenesis. Previous studies showed that lncRNA AFAP1-AS1 was aberrantly expressed in numerous cancers. Nevertheless, we know quite a little about the expression pattern and biological function of AFAP1-AS1 in thyroid cancer. In this study, we adopted the quantitative real-time PCR (qRT-PCR) to detect the expression of AFAP1-AS1 in thyroid cancer tissues. We discovered that expression of AFAP1-AS1 was increased in thyroid cancer tissues. MTT assays elucidated that down-regulation of AFAP1-AS1 could suppress growth of thyroid cancer cells. And the results of flow cytometry analysis indicated knockdown of AFAP1-AS1 induced apoptosis in thyroid cancer. Transwell assay was applied to show decreased cell migration in thyroid cancer as a result of down-regulation of AFAP1-AS1. Hence, our study provided evidence for our hypothesis that AFAP1-AS1 could be a therapeutic target for thyroid cancer. 

Retracted: No

PubPeer comments:
 Figure 3A. Rather unexpectedly, some parts of the flow cytometry panels appear to be visible in other panels as well. Boxes of the same color highlight areas that look similar. ![file] , 
 An additional finding in Figure 4. * Blue boxes: two panels appear to overlap. ![file] ,
Insulin receptor substrates Irs1 and Irs2 coordinate skeletal muscle growth and metabolism via the Akt and AMPK pathways
Authors: Zhiyong Cheng
Yun Chau Long
Morris F White
Kyle D Copps
Journal: Molecular and Cellular Biology (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: skeletal muscle growth; metabolism; insulin-like signaling; Irs1; Irs2
Affiliations: Howard Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Center for Life Sciences, CLS-16020, 3 Blackfan Circle, Boston, MA 02115, USA., Howard Hughes Medical Institute, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115

Abstract:  Coordination of skeletal muscle growth and metabolism with nutrient availability is critical for metabolic homeostasis. To establish the role of insulin-like signaling in this process, we used muscle creatine kinase (MCK)-Cre to disrupt expression of insulin receptor substrates Irs1 and Irs2 in mouse skeletal/cardiac muscle. In 2-week-old mice, skeletal muscle masses and insulin responses were slightly affected by Irs1, but not Irs2, deficiency. In contrast, the combined deficiency of Irs1 and Irs2 (MDKO mice) severely reduced skeletal muscle growth and Akt→mTOR signaling and caused death by 3 weeks of age. Autopsy of MDKO mice revealed dilated cardiomyopathy, reflecting the known requirement of insulin-like signaling for cardiac function (P. G. Laustsen et al., Mol. Cell. Biol. 27:1649-1664, 2007). Impaired growth and function of MDKO skeletal muscle were accompanied by increased Foxo-dependent atrogene expression and amino acid release. MDKO mice were resistant to injected insulin, and their isolated skeletal muscles showed decreased insulin-stimulated glucose uptake. Glucose utilization in MDKO mice and isolated skeletal muscles was shifted from oxidation to lactate production, accompanied by an elevated AMP/ATP ratio that increased AMP-activated protein kinase (AMPK)→acetyl coenzyme A carboxylase (ACC) phosphorylation and fatty acid oxidation. Thus, insulin-like signaling via Irs1/2 is essential to terminate skeletal muscle catabolic/fasting pathways in the presence of adequate nutrition. 

Retracted: No

PubPeer comments:
 The XRPD part is totally incredible. See the  powder patterns ... The compounds are amorphous, at best, so the  indexed cell parameters are crazyfool : ![file] ![file] ,
miR-154 suppresses non-small cell lung cancer growth in vitro and in vivo
Authors: Peng Zhang
Xingyu Lin
Guoguang Shao
Zhiguang Yang
Journal: Oncology Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: miR-154; tumor suppressor; non-small cell lung cancer (NSCLC); tumorigenesis; development
Affiliations: Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Anesthesiology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract:  miR-154 has been proven to act as a tumor suppressor in several types of tumors. However, its role in non-small cell lung cancer (NSCLC) remains unclear. Thus, the aim of this study was to investigate the effects of miR-154 on NSCLC tumorigenesis and development. Using real-time quantitative PCR (qRT-PCR), we analyzed expression of miR-154 at the transcriptional level in 40 NSCLC tumor tissues and matched adjacent normal tissues and the correlation with clinicopathological features of the patients. The miR-154 mimic was stably transfected into NSCLC A549 cells, and the effects of miR-154 on cancer cell proliferation, colony formation, cell cycle arrest, apoptosis, migration and invasion in vitro, and on the growth of in vivo xenografts were investigated. miR-154 expression levels were significantly downregulated in the NSCLC compared to the corresponding non-cancerous lung tissues (P&lt;0.05), and decreased miR-154 expression was significantly associated with metastasis (P&lt;0.001), larger tumor size (P&lt;0.001) and advanced TNM stage (P&lt;0.001). Furthermore, transfection of the miR-154 mimic into the NSCLC A549 cells was able to inhibit cell proliferation, colony formation, invasion and migration, and induce cell apoptosis and G0/G1 cell cycle arrest. Enforced expression of miR-154 also suppressed the growth of cancer cell xenografts in vivo. These findings indicate that miR-154 may become a potential target for miR-based therapy of NSCLC. 

Retracted: No

PubPeer comments:
 *[left]* Fig 5.  Upregulation of miR-154 results in increased E-cadherin expression, and decreased N-cadherin and vimentin expression in the A549 cells trans-fected with the miR-154 mimic as analyzed by western blot analysis. *[right]* Fig 5D of [Liu et al (2016)] .  The ADAM10 protein expression was measured in four HCC cell lines (SMMC-7721, Hep3B, HepG2, Huh-7) and normal hepatic cell line HL-7702 by western blot . Flipped horizontally for easier comparison of the bands marked in pink rectangles. ![file] Red and green rectangles: see *[left]* Fig 1C from [Pan et al (2015)] .  Western blot analysis for STAT3 and LKB1 in SKVO3 cells transfected with different recombinant treatment plasmids. *[right]* Fig 1C from [Zhang et al (2015)] .  Western blot analysis of the protein expression of GRIM-19 72 h after transfection. ![] The other bands are also familiar members of this *dramatis personae* but I will not belabour the point. ,
MiR-503 inhibits hepatocellular carcinoma cell growth via inhibition of insulin-like growth factor 1 receptor
Authors: Jiantai He
Ming Huang
Qinggang Tian
Liansheng Gong
Yao Xiao
Chao Yang
Journal: OncoTargets and Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; hepatocellular carcinoma; insulin-like growth factor 1 receptor; microRNA-503; proliferation.
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China., Department of General Surgery, The Fourth Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, People's Republic of China.

Abstract:  MicroRNAs (miRs) have been demonstrated to play key roles in the development and progression of hepatocellular carcinoma (HCC). However, the regulatory mechanism of miR-503 in HCC has not been fully uncovered. In this study, we found that miR-503 was significantly downregulated in HCC tissues compared to nontumorous liver tissues. Moreover, lower miR-503 levels were associated with the malignant progression of HCC, and the expression of miR-503 was also decreased in several common HCC cell lines compared to normal human liver cell line THLE-3. Overexpression of miR-503 inhibited proliferation but induced apoptosis of LM3 and HepG2 cells. Bioinformatical analysis and luciferase reporter assay further identified insulin-like growth factor 1 receptor (IGF-1R) as a novel target of miR-503 in 293T cells. Moreover, overexpression of miR-503 led to a significant decrease in the protein levels of IGF-1R, while knockdown of miR-503 enhanced its protein levels in LM3 and HepG2 cells. Besides, overexpression of IGF-1R reversed the effects of miR-503-mediated HCC cell proliferation and apoptosis, indicating that IGF-1R acts as a downstream effector of miR-503 in HCC cells. Furthermore, IGF-1R was found to be significantly upregulated in HCC tissues compared to nontumorous liver tissues. In addition, the mRNA levels of IGF-1R were inversely correlated to the miR-503 levels in the HCC tissues. Thus, we demonstrate that miR-503 inhibits the proliferation and induces the apoptosis of HCC cells, partly at least, by directly targeting IGF-1R, and suggest that IGF-1R may serve as a promising target for the treatment of HCC. 

Retracted: No

PubPeer comments:
 *[left[* Fig 3G.  the protein levels of IGF-1R were then examined using Western blot assay . Unexpectedly similar to *[right]* Fig 3C from [Tan et al (2016)] .  Western blotting was conducted to examine the protein expression levels of LIMK1 in H460 cellz transfected with miR-138 mimics or a miR-138 inhibitor (after a vertical flip). ![file] Other manifestations include *[left]* Fig 4D from [Zhou et al (2016)] ,  Western blot was used to examine the protein levels of EMT-related genes ; and *[right]* Fig 6F from [Hu et al (2016)] ,  Western blot assay was conducted to examine the protein expression of LASP1, Ki67, and MMP2 in xenografted tumor tissues . Vertically stretched to facilitate comparison. ![file] ,
Focal adhesion kinase controls actin assembly via a FERM-mediated interaction with the Arp2/3 complex
Authors: Gareth E Jones
Alan Serrels
Margaret C Frame
Bryan Serrels
Gordon W McLean
Christopher H Gray
Mark Holt
Valerie G Brunton
Journal: Nature Cell Biology (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: actin filaments; Arp2/3 complex; cell migration; integrins; focal adhesion kinase (FAK)
Affiliations: The Beatson Institute for Cancer Research, Cancer Research UK Beatson Laboratories, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.

Abstract:  Networks of actin filaments, controlled by the Arp2/3 complex, drive membrane protrusion during cell migration. How integrins signal to the Arp2/3 complex is not well understood. Here, we show that focal adhesion kinase (FAK) and the Arp2/3 complex associate and colocalize at transient structures formed early after adhesion. Nascent lamellipodia, which originate at these structures, do not form in FAK-deficient cells, or in cells in which FAK mutants cannot be autophosphorylated after integrin engagement. The FERM domain of FAK binds directly to Arp3 and can enhance Arp2/3-dependent actin polymerization. Critically, Arp2/3 is not bound when FAK is phosphorylated on Tyr 397. Interfering peptides and FERM-domain point mutants show that FAK binding to Arp2/3 controls protrusive lamellipodia formation and cell spreading. This establishes a new function for the FAK FERM domain in forming a phosphorylation-regulated complex with Arp2/3, linking integrin signalling directly with the actin polymerization machinery. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar and different than expected. ![file] , 
 ![file] , 
 #2 How to explain that the FAK panels are very similar (after horizontal stretching), yet the accompanying Arp3 panels are different? , 
 The FAK panels are the same blot and FAK was only blotted once from these lysates. The Arp3 expression blots (from exact same lysates) showing that there is consistently no difference in expression levels depending on FAK expression was done more than once, and different blots are shown in this case I see. , 
  The FAK panels are the same blot and FAK was only blotted once from these lysates. Many thanks for confirming that the FAK blots are the same.  The Arp3 expression blots (from exact same lysates) showing that there is consistently no difference in expression levels depending on FAK expression was done more than once, and different blots are shown in this case I see. The problem is that different Arp3 blots have been paired with the same FAK blot. This leads readers to assume that they have been run on the same gel and are directly comparable. , 
 Same cell lysates split and run on different gels blotted and probed with either anti-FAK or Anti-Arp3. 2a and 2b all the same experiment. Sorry if confusing. , 
 #6 It s more than confusing. The same FAK image should only be grouped with one Arp3 image, not with two. Supplementary Information. https: static-content.springer.com esm art%3A10.1038%2Fncb1626 MediaObjects 41556_2007_BFncb1626_MOESM2_ESM.pdf ![file] ,
Resource plasticity-driven carbon-nitrogen budgeting enables specialization and division of labor in a clonal community
Authors: Sunil Laxman
Adhish Walvekar
Sandeep Krishna
Sriram Varahan
Vaibhhav Sinha
Journal: eLife (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: S. cerevisiae; aspartate; cross-feeding; division of labor; glycolysis
Affiliations: InStem - Institute for Stem Cell Science and Regenerative Medicine, Bangalore, India., Simons Centre for the Study of Living Machines, National Center for Biological Sciences, Tata Institute for Fundamental Research, Bangalore, India., Manipal Academy of Higher Education, Manipal, India.

Abstract:  Previously, we found that in glucose-limited Saccharomyces cerevisiae colonies, metabolic constraints drive cells into groups exhibiting gluconeogenic or glycolytic states. In that study, threshold amounts of trehalose - a limiting, produced carbon-resource, controls the emergence and self-organization of cells exhibiting the glycolytic state, serving as a carbon source that fuels glycolysis (Varahan et al., 2019). We now discover that the plasticity of use of a non-limiting resource, aspartate, controls both resource production and the emergence of heterogeneous cell states, based on differential metabolic budgeting. In gluconeogenic cells, aspartate is a carbon source for trehalose production, while in glycolytic cells using trehalose for carbon, aspartate is predominantly a nitrogen source for nucleotide synthesis. This metabolic plasticity of aspartate enables carbon-nitrogen budgeting, thereby driving the biochemical self-organization of distinct cell states. Through this organization, cells in each state exhibit true division of labor, providing growth/survival advantages for the whole community. 

Retracted: No

PubPeer comments:
 Images have been reused in multiple figures. ![file] , 
 Same images have been reused in several figures all through the manuscript. Was it all just one experiment ? clarification from the authors would be appreciated. Why use same images in multiple figures, were the experiments replicated? ![file] ![file] ![file] ,
RETRACTED ARTICLE: Formaldehyde inhibits proliferation of bronchial epithelial cells by down-regulating miR-375
Authors: Lei Yu
ChunWen Li
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Formaldehyde; KLF4; bronchial epithelial cells; miR-375; proliferation.
Affiliations: a Department of Emergency, The Second Affiliated Hospital, Chongqing Medical University , Chongqing , China.

Abstract:  Objective: To study the effect of formaldehyde on the proliferation of human bronchial epithelial cells 16HBE and to explore its mechanism. Methods: MTT assay was used to detect the inhibition rate of formaldehyde-treated 16HBE cells; FCOH + miR-375 group (transfected miR-375 mimics), FCOH + miR-con group (transfected miR-con), FCOH + si-KLF4 group (transfected si-KLF4) and FCOH + si-con group (transfected si-con), were transfected into 16HBE cells by liposome method, then treated with formaldehyde 200 μmol/L for 24 h; qRT-PCR was used to detect the expression of miR-375 in each group; the protein expression of KLF4 in each group was detected by Western blot. The fluorescence activity of each group was detected by dual-fluorescein gene detection assay. Results: Compared with 16HBE cells in Control group, the expression of miR-375 was significantly decreased in FCOH group, cell proliferation was significantly decreased, and KLF4 expression was significantly increased (p &lt; .05). Overexpression of miR-375 and KLF4 knockdown could reverse the inhibition effect of formaldehyde on proliferation of 16HBE cells; KLF4 is a target of miR-375. KLF4 could reverse the promotion of miR-375 on the proliferation of formaldehyde-treated 16HBE cells. Conclusion: Formaldehyde can inhibit the proliferation of human bronchial epithelial cells. The mechanism may be related to the down-regulation of miR-375 targeting KLF4, which will provide support for the treatment of chronic respiratory diseases. 

Retracted: Yes

PubPeer comments:
 Retracted [11 January 2021] . ----------------------------------------- We, the Editors and Publisher of the journal Artificial Cells, Nanomedicine, and Biotechnology, have retracted the following article: Lei Yu ChunWen Li (2019) Formaldehyde inhibits proliferation of bronchial epithelial cells by down-regulating miR-375. Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 2293u20132297, DOI: 10.1080 21691401.2019.1624369 It has come to our attention that the full authorship list and affiliations for this manuscript were changed after the article was submitted. We have contacted the corresponding author for an explanation, but we have not received a satisfactory explanation. As determining authorship is core to the integrity of published work, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. ,
Protein typing of major outer membrane lipoproteins from Chinese pathogenic Leptospira spp. and characterization of their immunogenicity
Authors: Xuai Lin
Liwei Li
Feng Xue
Jie Yan
Dongjiao Luo
Yafei Mao
David M Ojcius
Jinfang Zhao
Journal: Vaccine (2009)
Discipline: IMMUNOLOGY
Keywords: Leptospirosis; Leptospira species; lipoproteins; immunogenicity; lipL21
Affiliations: Department of Medical Microbiology and Parasitology, College of Medicine, Zhejiang University, 388 Yuhangtang Road, Hangzhou, Zhejiang 310058, PR China. 

Abstract:  Leptospirosis, caused by different Leptospira species, is one of the most widespread zoonotic infections worldwide. Here we expressed three major leptospiral lipoproteins and examined their immunogenicity. All the pathogenic Leptospira strains tested possess the lipL21, lipL32 and lipL41 genes, but the latter two can be further divided into different gene types (lipL32-1, lipL32-2, lipL41-1, lipL41-2). Microscopic agglutination test revealed that rLipLs antisera had extensive cross-immunoagglutination among the 178 leptospiral strains in which rLipL32-1 contributed the highest agglutination titer. The rLipLs-based ELISAs established in this study demonstrated that in the sera of 385 leptospirosis patients infected with different serovars of Leptospira interrogans, rLipL32-1 had the highest positive rates for IgG and IgM (89.4-98.7%), followed by the IgG/IgM positive rates of rLipL21 (87.0-96.1%) and rLipL32-2 (86.5-96.9%), while the two rLipL41s presented the lowest IgG/IgM positive rates (69.9-83.9%). The immunoprotective levels in guinea pigs of rLipL32-1 (58.3% and 66.7%) were the highest, compared to those of the other rLipLs (25.0-58.3%). Multiple different rLipLs would increase immunoprotective levels (from 58.3% and 66.7% to 83.3% and 91.7%). The data suggest that all the rLipLs are the genus-specific superficial antigens of pathogenic Leptospira species and should be considered in designing universal vaccines against leptospirosis. 

Retracted: No

PubPeer comments:
 Concern about Figure 5, left panel. Some parts of the lanes look more similar to each other than expected. Some bands also appear to have unexpected sharp edges or peculiar placement that does not match the direction of the surrounding bands. Boxes of the same color highlight areas that look quite similar to each other. ![file] Here is a false color version of the image generated in FIJI ImageJ to show the similarities. ![file] It would be appreciated if the authors still might have the original blot to show here, to take away any concerns. , 
 #1 Thank you for your comment. We are repeating the experiment and will contact the journal for advice. , 
 Taking up my previous comment that was moderated. There are 3 figures, in 3 different papers with overlapping authors, that have features in common with the one in Dr. Bik s comment. I think that she is more experienced that me and that she can analyze them and highlight the similarities better that how I have done it - that seems not to reach the standards of Pubpeer. So I just post them. ![file] ![file] ![file] ,
Association of pro‐ and anti‐inflammatory cytokines in preeclampsia
Authors: Mangala Kohli
Pratima Mittal
Arun Kumar Jain
Gayatri Rath
Poonam Jawanjal
Ruby Aggarwal
Journal: Journal of Clinical Laboratory Analysis (2019)
Discipline: CLINICAL MEDICINE
Keywords: IL-10; IL-4; IL-6; TNF-α; cytokines
Affiliations: Department of Anatomy, Vardhman Mahavir Medical College & Safdarjung Hospital, New Delhi, India., National Institute of Pathology (ICMR), New Delhi, India., Department of Obstetrics and Gynecology, Vardhman Mahavir Medical College & Safdarjung Hospital, New Delhi, India.

Abstract:  Introduction: The pro- and anti-inflammatory cytokines play crucial role in the development and functions of placenta. Any changes in these cytokines may be associated with many pregnancy-related disorders like preeclampsia. Therefore, the present study is aimed to study the expression of pro-inflammatory (TNF-α, IL-6) and anti-inflammatory (IL-4, IL-10) cytokines in placenta and serum of preeclamptic pregnant women. Material and methods: For this study, a total of 194 cases of preeclamptic and control cases were enrolled in two Groups as per the gestational age that is, Group I (28-36 weeks) and II (37 weeks onwards). The number of samples was 55 in Group I and 139 in Group II. The immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA) were conducted on placenta and serum of both preeclamptic and normal samples, respectively. IHC results were revalidated by reverse transcriptase PCR (RT-PCR). Results: Both Groups (I, II) of preeclampsia showed amended levels of pro- and anti-inflammatory cytokines in placental tissues and serum samples. The levels of TNF-α and IL-6 were significantly increased in preeclamptic cases (P = 0.0001, P = 0.0001) while the IL-4 and IL-10 were downregulated (P = 0.0001, P = 0.0001) in comparison to control. In addition, a negative correlation was also observed between the two in preeclampsia (P = 0.0001). Conclusion: The balanced ratio of pro- and anti-inflammatory cytokines is essential to regulate the maternal inflammation system throughout pregnancy. Therefore, the gradual cytokine profiling of the pregnant women may be useful for the management of preeclampsia. 

Retracted: No

PubPeer comments:
 Dear authors, Thank you for an interesting paper. Please forgive if it is stated somewhere, but I was unable to find how many of your participants that developed preeclampsia in each group and in total. Could you please provide these numbers? To interpret your findings, we need to know how many controls there were compared to the number of cases ,
De novo induction of amyloid-β deposition in vivo
Authors: L D Estrada
R Morales
C Soto
C Duran-Aniotz
J Castilla
Journal: Molecular Psychiatry (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer's disease; senile dementia; misfolded amyloid-β; Aβ accumulation; brain extracts
Affiliations: Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA.

Abstract:  Alzheimer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfolded amyloid-β (Aβ) in the brain. Although compelling evidences indicate that the misfolding and oligomerization of Aβ is the triggering event in AD, the mechanisms responsible for the initiation of Aβ accumulation are unknown. In this study, we show that Aβ deposition can be induced by injection of AD brain extracts into animals, which, without exposure to this material, will never develop these alterations. The accumulation of Aβ deposits increased progressively with the time after inoculation, and the Aβ lesions were observed in brain areas far from the injection site. Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. 

Retracted: No

PubPeer comments:
 Identified by another reader. ** ![file] The authors would like to correct a labeling mistake in Figure 4 of the article. The top two panels in the left (developed with anti-Au03b2 antibody) correspond to an animal killed at 450 days post inoculation and not 585 days as stated in the labeling. Indeed, the panel shown at u00d7 200 magnification corresponds to a new picture taken with higher resolution of the same section shown in Figure 3a (center panel). The other two top panels in the right (stained with thioflavin S and anti-GFAP antibody, respectively) are correctly labeled as coming from an animal killed at 585 days post inoculation. This mistake does not affect in any way the results or conclusions of the experiment, as the purpose of Figure 4 was to show a morphological and staining comparison of representative deposits observed in HuAPPwt transgenic mice after inoculation with Alzheimer s brain homogenate and those developed spontaneously in a mice expressing human mutant amyloid precursor protein (Tg2576). ,
Thyroid hormones directly activate the expression of the human and mouse uncoupling protein-3 genes through a thyroid response element in the proximal promoter region
Authors: Neus Pedraza
Francesc Villarroya
Antonio Vidal-Puig
Bradford B Lowell
Verónica Calvo
Gemma Solanes
Journal: Biochemical Journal (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: UCP3 gene; thyroid hormones; skeletal muscle; transcription; metabolic signals
Affiliations: Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Avda Diagonal 645, E-08028 Barcelona, Spain. , Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Avda Diagonal 645, E-08028 Barcelona, Spain, Department of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, MA 02115, U.S.A., Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QR, U.K.

Abstract:  The transcription of the human UCP3 (uncoupling protein-3) gene in skeletal muscle is tightly regulated by metabolic signals related to fatty acid availability. However, changes in thyroid status also modulate UCP3 gene expression, albeit by unknown mechanisms. We created transgenic mice bearing the entire human UCP3 gene to investigate the effect of thyroid hormones on human UCP3 gene expression. Treatment of human UCP3 transgenic mice with thyroid hormones induced the expression of the human gene in skeletal muscle. In addition, transient transfection experiments demonstrate that thyroid hormones activate the transcription of the human UCP3 gene promoter when MyoD and the TR (thyroid hormone receptor) were co-transfected. The action of thyroid hormones on UCP3 gene transcription is mediated by the binding of the TR to a proximal region in the UCP3 gene promoter that contains a direct repeat structure. An intact DNA sequence of this site is required for thyroid hormone responsiveness and TR binding. Chromatin immunoprecipitation assays revealed that the TR binds this element in vivo. The murine Ucp3 gene promoter was also dependent on MyoD and responsive to thyroid hormone in transient transfection assays. However, it was much less sensitive to thyroid hormone than the human UCP3 promoter. In summary, UCP3 gene transcription is activated by thyroid hormone treatment in vivo, and this activation is mediated by a TRE (thyroid hormone response element) in the proximal promoter region. Such regulation suggests a link between UCP3 gene expression and the effects of thyroid hormone on mitochondrial function in skeletal muscle. 

Retracted: No

PubPeer comments:
 Figure 6. Much more similar than expected. ![file] ,
KLF4 suppresses the migration of hepatocellular carcinoma by transcriptionally upregulating monoglyceride lipase
Authors: Wanglai Hu
Dongmei Zhang
Xiaojie Li
Sha Liu
Chuanchun Han
Xuejun Yang
Journal: American journal of cancer research (2018)
Discipline: CLINICAL MEDICINE
Keywords: KLF4; MGLL; hepatocellular carcinoma; lipid metabolism; migration.
Affiliations: Institute of Cancer Stem Cell and Department of General Surgery of The First Affiliated Hospital of Dalian Medical University Dalian 116044, China., Department of Physiology of College of Basic Medical Science, College of Stomatology of Dalian Medical University Dalian 116044, China., Department of Immunology, Anhui Medical University Hefei 230032, China.

Abstract:  The dysregulation of cellular metabolism, particularly lipid metabolism, is essential for cancer progress. Monoglyceride lipase (MGLL) is an important fatty acid metabolism enzyme, which converts monoacylglycerides to free fatty acids and glycerol. Despite the expression level of MGLL was reported to be downregulated in Hepatocellular carcinoma (HCC), the clinical significances and molecular mechanism of MGLL downregulation remains unknown. In the current study, the clinical significances of MGLL expression were investigated in 95 patients with HCC and the transcription factors of MGLL were identified in HCC cells. We found that MGLL was frequently downregulated in HCC samples, especially in metastatic tumor tissues. Patients with low MGLL expression owned remarkably lower 5 year-overall survival (5-OS). Functionally, we found that MGLL played an important role in HCC cell migration. Overexpression of MGLL suppressed cell migration and depletion of MGLL by shRNA promoted cell migration. Further studies indicated that KLF4 directly bound to the promoter of MGLL and accelerated MGLL expression, which then led to HCC cell migration decrease. Additionally, the expression levels of KLF4 were positive association with MGLL expression in HCC tissues. Collectively, our data suggest that KLF4 is a key regulator of MGLL. The KLF4-MGLL axis plays an essential role in suppressing HCC cell migration. 

Retracted: No

PubPeer comments:
 Several images in Figure 2B and 2G appear to overlap. Dotted lines indicate possible partial overlaps. TAM. *** ![file] ,
Buyang Huanwu Decoction Ameliorates Poststroke Depression via Promoting Neurotrophic Pathway Mediated Neuroprotection and Neurogenesis
Authors: Jian Yi
Yan She
Sainan Zhou
Baiyan Liu
Shuhua Deng
Lin Luo
Journal: Evidence-based Complementary and Alternative Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: Buyang Huanwu Decoction; poststroke depression; neurotrophic pathway; neuroprotection; neurogenesis
Affiliations: Hunan University of Chinese Medicine, Changsha, Hunan 410208, China

Abstract:  Objective. The aim of the present research is to investigate the therapeutic effect of Buyang Huanwu Decoction (BHD) in poststroke depression (PSD) animal model and illustrate its underlying mechanism via promoting neurotrophic pathway mediated neuroprotection and neurogenesis. Methods. To induce PSD rat model, isolation housed rats that received middle cerebral artery occlusion (MCAO) surgery successively suffered from chronic mild stress (CMS) treatment for consecutive twenty-one days. Meanwhile, rats were correspondingly given vehicle, BHD, and fluoxetine. Then, neurologic function was scored and depressive-like behaviors were assessed by sucrose preference test, locomotor activity, novelty-suppressed feeding test, and forced swim test. Thereafter, the neuroprotection and neurogenesis related molecular markers and signaling were detected. Results. We firstly observed a significant neurological function recovery and antidepressants effect of BHD after MCAO together with CMS treatment. Our study also found that treatment with BHD and fluoxetine can significantly rescue neurons from apoptosis and promote neurogenesis in the CA3 and DG regions in the hippocampus. Notably, BHD and fluoxetine treatment can activate BDNF/ERK/CREB signaling. Conclusion. The results suggest that BHD is a promising candidate for treating PSD. Its curative effects can be attributed to neurotrophic pathway mediated neuroprotection and neurogenesis. 

Retracted: No

PubPeer comments:
 There is an image duplication in Figure 4, where two of the panels are of the same histology slide. One has been resized, cropped and rotated, however. ![file] ,
p53 suppresses stress-induced cellular senescence via regulation of autophagy under the deprivation of serum
Authors: Xinbing Sui
Haizhou Lou
Wei Chen
Hongming Pan
Fang Lou
Yong Fang
Kaifeng Wang
Yinghua Xu
Xian Wang
Weidong Han
Wei Jin
Yu Zheng
Journal: Molecular medicine reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: p53; tumor suppressor; autophagy; senescence; cell cycle arrest
Affiliations: Department of Medical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, Zhejiang 310016, P.R. China.

Abstract:  The tumor suppressor p53 is widely known for its ability to induce cell cycle arrest or cell death, therefore preventing neoplastic progression. Previous studies have demonstrated novel roles for p53 in the regulation of autophagy and senescence. p53 can not only exert cell cycle‑arresting and senescence‑promoting or suppressing functions, but can also induce autophagic ﬂux, particularly under conditions of nutrient deprivation. The present study demonstrated that p53 was capable of activating autophagy, which permits cell survival under conditions of serum starvation, and suppresses cellular senescence through inhibition of the mammalian target of rapamycin pathway. These results suggest that active autophagy may be a potential mechanism by which p53 suppresses cellular senescence, in response to serum starvation. The findings of the present study provide a potential mechanism for suppression of senescence by p53. 

Retracted: Yes

PubPeer comments:
 DUPLICATION! ![file] , 
 Graphical reference (cover page) for the above (plagiarized) paper *[Left]*! Number of authors changed from **8** *[Right]* to **2** *[Left]* **(vice versa)** in the above process of publication without a major difference in the works! ![file] ,
Nanoscale Metal-Organic Framework Mediates Radical Therapy to Enhance Cancer Immunotherapy
Authors: Wenbin Lin
Nina Fatuzzo
Theint Aung
Kaiyuan Ni
Shuyi Li
Xingjie Liang
Journal: Chem (2019)
Discipline: CHEMISTRY
Keywords: checkpoint blockade immunotherapy; chemodynamic therapy; hormone therapy; metal-organic frameworks; photodynamic therapy.
Affiliations: Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA.

Abstract:  Checkpoint blockade immunotherapy (CBI) elicits durable therapeutic responses by blocking T cell inhibitory pathways of tumors with pre-infiltrated T cells and/or high mutational burden to activate antitumor immunity but is ineffective against poorly immunogenic tumors. Immunogenic radiotherapy, photodynamic therapy (PDT), and chemotherapy have thus been examined as immunomodulatory adjuvants to augment CBI. Dysregulated hormone production has long been linked to tumorigenesis and poor prognosis of various cancers. Herein, we report the use of a Cu-porphyrin nanoscale metal-organic framework (nMOF) to mediate synergistic hormone-triggered chemodynamic therapy (CDT) and light-triggered PDT. The combination of CDT/PDT-based radical therapy with a programmed cell-death ligand 1 blockade effectively extends the local therapeutic effects of CDT/PDT to distant tumors via abscopal effects on mouse tumor models with high levels of estradiol. Our work thus establishes the feasibility of combining nMOF-mediated radical therapy with CBI to elicit systemic antitumor immunity in hormonally dysregulated tumor phenotypes. 

Retracted: No

PubPeer comments:
 Multiple duplication areas were observed from the following images: 1. Figure 1 L, Cu-TBP (1 h) vs. H4-TBP (4 h). ![file] 2. Figure 2, PBS (merged) vs. H4-TBP (merged) ![file] 3. Figure S22, PBS (live) vs. Cu-TBP (live). ![file] , 
 Dear Pubpeer readers, We are launching an investigation into this matter and will get to the bottom of this matter. We will report our findings and work with the journals to address the problems. As the corresponding author of these problematic papers, I apologize for my failure to catch potential misconducts of a singular former graduate student in my lab. Wenbin ,
Anal swab as a potentially optimal specimen for SARS-CoV-2 detection to evaluate hospital discharge of COVID-19 patients
Authors: Peng Liu
Ming-Yi Wang
Dong Guo
Mei Sun
Hai-Feng Teng
Jing Zhang
Jun Xia
Jian Zhang
Quan-Xu Ge
Journal: Future Microbiology (2020)
Discipline: MICROBIOLOGY
Keywords: COVID-19; RT-PCR; SARS-CoV-2; anal swab.
Affiliations: Department of Central Lab, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong 264200, PR China, Department of Infectious Diseases, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong 264200, PR China, Department of Intensive Care Unit, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong 264200, PR China, Department of Infectious Diseases, Weihai Chest Hospital. Weihai, Shandong 264200, PR China, Department of Radiology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong 264200, PR China

Abstract:  Since December 2019, an outbreak of SARS coronavirus 2 (SARS-CoV-2) began in Wuhan, and has rapidly spread worldwide. Previously, discharged patients with coronavirus disease 2019 (COVID-19) patients met the criteria of China's pneumonia diagnosis and treatment program of novel coronavirus infection (trial version 7) for cure of viral infection. Nevertheless, positive detection of SARS-CoV-2 has been found again in several cured COVID-19 patients, leading to conflicts with current criteria. Here, we report clinically cured cases with positive results only in anal swabs, and investigate the clinical value of anal swabs for SARS-CoV-2 detection. 

Retracted: Yes

PubPeer comments:
 *[above]* Figure 5 from [Zhu et al (2019)] .  Overexpression of CUL-5 inhibits proliferation, migration and invasion of SNU-16 cells...The effect of CUL5 overexpression on... (C) colony formation . *[below]* Fig 4C from [Si et al (2019)] .  Colony formation of NC and pcDNA-CUL5 transfected SK-OV3 and OVACAR-3 cells . ![file] , 
 *[left]* Figure 7C.  Effects of CUL-5 silencing (Si-CUL5) overexpression on ... (C) migratory and invasive abilities of miR-19a inhibitor transfected SNU-16 cells. *[right]* Figure 7 from [Chen, Lu Hu (2019)] .  Transwell assay showing the invasion of the miRNC and miR-299 mimic-transfected HK1 nasopharyngeal cancer cells . ![file] ,
3-Bromopyruvate induces apoptosis in breast cancer cells by downregulating Mcl-1 through the PI3K/Akt signaling pathway
Authors: Cheng-Zhu Wu
Su-Rong Zhao
Yuan-Yuan Zhang
Chen-Chen Jiang
Hao Liu
Xiu Cheng
Zhe Liu
Qian-Wen Zhang
Zhi-Wen Jiang
Journal: Anti-Cancer Drugs (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: 3-bromopyruvate; glycolysis; ATP production; apoptosis; alkylating agent
Affiliations: aFaculty of Pharmacy, Bengbu Medical College, Bengbu, Anhui, People's Republic of China bSchool of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.

Abstract:  The hexokinase inhibitor 3-bromopyruvate (3-BrPA) can inhibit glycolysis in tumor cells to reduce ATP production, resulting in apoptosis. However, as 3-BrPA is an alkylating agent, its cytotoxic action may be induced by other molecular mechanisms. The results presented here reveal that 3-BrPA-induced apoptosis is caspase independent. Further, 3-BrPA induces the generation of reactive oxygen species in MDA-MB-231 cells, leading to mitochondria-mediated apoptosis. These results suggest that caspase-independent apoptosis may be induced by the generation of reactive oxygen species. In this study, we also demonstrated that 3-BrPA induces apoptosis through the downregulation of myeloid cell leukemia-1 (Mcl-1) in MDA-MB-231 breast cancer cells. The results of Mcl-1 knockdown indicate that Mcl-1 plays an important role in 3-BrPA-induced apoptosis. Further, the upregulation of Mcl-1 expression in 3-BrPA-treated MDA-MB-231 cells significantly increases cell viability. In addition, 3-BrPA treatment resulted in the downregulation of p-Akt, suggesting that 3-BrPA may downregulate Mcl-1 through the phosphoinositide-3-kinase/Akt pathway. These findings indicate that 3-BrPA induces apoptosis in breast cancer cells by downregulating Mcl-1 through the phosphoinositide-3-kinase/Akt signaling pathway. 

Retracted: No

PubPeer comments:
 In order to ensure the accuracy of the scientific record, we checked the raw data recently. We found that these is a picture misuse in Fig 5. The above error does not affect our conclusion, and we will contact the journal about this error as soon as possible. ,