PReD-Bench/PRed-Bench huggingface dataset:
Pathogenesis of leptospirosis: interaction of Leptospira interrogans with in vitro cultured mammalian cells
Authors: Yunying Liu
Liwei Li
Yafei Mao
Jie Yan
Wei Zheng
Journal: Medical Microbiology and Immunology (2007)
Discipline: IMMUNOLOGY
Keywords: Leptospira interrogans; host cells; attachment; internalization; morphological analysis
Affiliations: Department of Medical Microbiology and Parasitology, School of Medicine, Zhejiang University, Hangzhou, 310058, People's Republic of China.

Abstract:  Interactions of virulent Leptospira interrogans with murine monocyte-macrophage-like J774A.1 cells and Vero (African green monkey kidney fibroblasts) cells from attachment to internalization were investigated by a series of morphological analysis. Fontana silver staining revealed that only the pathogenic leptospires were able to attach to host cells and the attachment pattern varied depending on cell types that they interacted with. Transmission electron microscopy (TEM) analysis confirmed the formation of the leptospires-containing phagosomes and their colocalization with lysosomes in macrophages were verified by confocal microscopic analysis. Results of F-actin rearrangements examination indicated that virulent leptospires invaded host cells via a microfilament-independent pathway. 

Retracted: No

PubPeer comments:
 Authors from the same lab seemed reuse their images between papers. The same reused images did seem represent the same experimental condition. However, it is expected that the authors acknowledge the images were used previously in other of their publications. Additionally, Liu, et al 2007 Fig 1 didn t appear to have scale bars. The other paper (Li, et al 2007) is flagged in a different thread. https: pubpeer.com publications 4E45259AF3F99848041ECBD7432C05#1 ![] ![] , 
 Found another duplication between them, although there are two spots different. ![file] ![file] ,
<p>Glucosamine-6-Phosphate Isomerase 1 Promotes Tumor Progression and Indicates Poor Prognosis in Hepatocellular Carcinoma</p>
Authors: Xianyi Cheng
Dezhi Li
Junhui Chen
Wei Zheng
Journal: Cancer management and research (2020)
Discipline: CLINICAL MEDICINE
Keywords: glucosamine-6-phosphate isomerase 1; hepatocellular carcinoma; poor prognosis; reprogramming of metabolic pathways.
Affiliations: Intervention and Cell Therapy Center, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, People's Republic of China., Department of Research and Development, Shenzhen Institute for Innovation and Translational Medicine, Shenzhen, Guangdong, People's Republic of China.

Abstract:  Purpose: Reprogramming of metabolic pathways is a hallmark of the pathological changes that occur in cancer cells. Under physiological conditions, glucosamine-6-phosphate isomerase 1 (GNPDA1) promotes the conversion of the hexosamine system to the glycolytic pathway and may, therefore, affect energy metabolism. Low expression of GNPDA1 has been reported in normal liver tissues, however, analysis of the hepatocellular carcinoma (HCC) database in The Cancer Genome Atlas (TCGA) revealed that GNPDA1 was highly expressed in HCC tissues. The purpose of this study was to explore the role of GNPDA1 in HCC. Patients and methods: We analyzed the expression of GNPDA1 in HCC tissues as well as the clinical outcomes of HCC patients with high or low expression of GNPDA1. Furthermore, the relationship between the expression of GNPDA1 and advanced tumor stage, TNM stage, grade, gender, or metastasis was assessed using high-throughput RNA sequencing data from TCGA HCC cohort and Kaplan-Meier survival analysis. The expression of GNPDA1 in HCC and normal liver cell lines was subsequently detected by qRT-PCR and Western blot analysis. Additionally, the effects of GNPDA1 knockdown in SMMC-7721 and Huh7 cell lines were examined. Cell proliferation, migration, invasion, and apoptosis following knockdown were investigated by the MTT assay and EdU, cell cycle, apoptosis, transwell, and wound healing analyses. Results: There was a significant association between high GNPDA1 expression and advanced tumor stage, TNM stage or grade, but not with gender. High GNPDA1 expression was associated with poor prognosis in patients with HCC. Furthermore, the MTT assay and EdU, cell cycle, apoptosis, wound healing, and transwell analyses revealed that GNPDA1 promoted the proliferation, migration, and invasion of HCC cells and inhibited apoptosis. Conclusion: The results of this study suggest that GNPDA1 may serve as a novel prognostic biomarker and therapeutic target for HCC. 

Retracted: No

PubPeer comments:
 Figure 5E appears to include a repeated image. *** ![file] , 
 The concern above has been corrected. *** ![file] , 
 Unfortunately, Figure 7 appears to have an image overlap, although the colors appear to have been altered, suggesting that this was not merely an error made during figure assembly. *** ![file] ,
RETRACTED ARTICLE: Modified box dimension and average weighted receiving time on the weighted fractal networks
Authors: Yanqiu Sun
Meifeng Dai
Shuxiang Shao
Weiyi Su
Lifeng Xi
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: Weighted fractal networks; Modified box dimension; Weighted factor; Number of copies; Average weighted receiving time (AWRT)
Affiliations: Nonlinear Scientific Research Center, Faculty of Science, Jiangsu University Zhenjiang, Jiangsu, 212013, P.R. China., Institute of Mathematics, Zhejiang Wanli University, Ningbo 315100, P.R. China., Department of Mathematics, Nanjing University, Nanjing, 210093, P. R. China.

Abstract:  In this paper a family of weighted fractal networks, in which the weights of edges have been assigned to different values with certain scale, are studied. For the case of the weighted fractal networks the definition of modified box dimension is introduced, and a rigorous proof for its existence is given. Then, the modified box dimension depending on the weighted factor and the number of copies is deduced. Assuming that the walker, at each step, starting from its current node, moves uniformly to any of its nearest neighbors. The weighted time for two adjacency nodes is the weight connecting the two nodes. Then the average weighted receiving time (AWRT) is a corresponding definition. The obtained remarkable result displays that in the large network, when the weight factor is larger than the number of copies, the AWRT grows as a power law function of the network order with the exponent, being the reciprocal of modified box dimension. This result shows that the efficiency of the trapping process depends on the modified box dimension: the larger the value of modified box dimension, the more efficient the trapping process is. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: doi.org 10.1038 s41598-020-63244-9 The Editors have retracted this Article because significant portions of the text and equations were taken from Roland Molontayu2019s BSc thesis without attribution1. The following parts of the paper are copied verbatim or are adapted from those appearing in the thesis: the definition of dB and preceding and subsequent sentences; Definition 3.2; Proof of Lemma 3.4; Lemma 3.5; Proof of Lemma 3.5; Lemma 3.6; Proof of Lemma 3.6; Equation 6; Lemma 3.7; Proof of Lemma 3.7; Lemma 3.8; Equation 8; Proof of Theorem 3.3. The authors do not agree to the retraction of the Article. Reference 1. Molontay, R. Networks and fractals. BSc thesis, Budapest University of Technology and Economics, http: math.bme.hu ~molontay Szakdolgozat.pdf (2013). ,
Retracted Article: Resveratrol attenuates inflammation and reduces matrix-metalloprotease expression by inducing autophagy via suppressing the Wnt/β-catenin signaling pathway in IL-1β-induced osteoarthritis chondrocytes
Authors: Haichun Liu
Wenliang Wu
Guangjun Jiao
Ci Li
Yunzhen Chen
Journal: RSC Advances (2018)
Discipline: CHEMISTRY
Keywords: Resveratrol; IL-1β; osteoarthritis; chondrocytes; inflammation
Affiliations: Department of Orthopedics, Qilu Hospital of Shandong University, Jinan 250012, China

Abstract:  Resveratrol (Res), a naturally occurring polyphenolic compound, has been reported to exert many biological effects like anti-inflammatory and anti-oxidant effects. In this study, we investigated the role of Res on IL-1β-induced osteoarthritis (OA) chondrocytes and its possible mechanism. Results demonstrated that Res suppressed IL-1β-induced IL-1, IL-6 and TNF-α production in a dose-dependent manner. Res also decreased MMP-1, MMP-3 and MMP-13 production in IL-1β-induced OA chondrocytes. These results suggested that Res suppressed IL-1β-induced inflammation and matrix-metalloproteases (MMP) expression in OA chondrocytes. In addition, Res was found to reverse the decreased autophagy level through increasing the expression of Beclin1, LC3 II/I ratio and LC3+ puncta in IL-1β-induced OA chondrocytes. Inhibition of autophagy by 3-methyladenine (3-MA) abolished the inhibitory effect of Res on inflammation and MMP expression in IL-1β-induced OA chondrocytes. Moreover, the Wnt/β-catenin signaling pathway was activated in IL-1β-induced OA chondrocytes. However, Res was found to suppress this activated Wnt/β-catenin signaling pathway. Activation of the Wnt/β-catenin signaling pathway counteracted the promoted effect on autophagy and inhibitory effect on inflammation and MMP expression of Res in IL-1β-induced OA chondrocytes. Taken together, our data demonstrated that Res attenuated inflammation and reduced MMP expression through inducing autophagy via inhibiting the Wnt/β-catenin signaling pathway in IL-1β-induced OA chondrocytes. Res may be used as a potential therapeutic agent for OA treatment. 

Retracted: Yes

PubPeer comments:
 This work was funded by a producer of ivermectin yet the COI section says there are no COI s What is this journal s policy on such matters? ,
Not4 E3 ligase contributes to proteasome assembly and functional integrity in part through Ecm29
Authors: Martine A Collart
Olesya O Panasenko
Journal: Molecular and Cellular Biology (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Not4; E3 ligase; proteasome integrity; polyubiquitinated proteins; free ubiquitin
Affiliations: Department of Microbiology and Molecular Medicine, University of Geneva, Faculty of Medicine, Geneva, Switzerland.

Abstract:  In this study we determine that the Not4 E3 ligase is important for proteasome integrity. Consequently, deletion of Not4 leads to an accumulation of polyubiquitinated proteins and reduced levels of free ubiquitin. In the absence of Not4, the proteasome regulatory particle (RP) and core particle (CP) form salt-resistant complexes, and all other forms of RPs are unstable. Not4 can associate with RP species present in purified proteasome holoenzyme but not with purified RP. Additionally, Not4 interacts with Ecm29, a protein that stabilizes the proteasome. Interestingly, Ecm29 is identified in RP species that are inactive and not detectable in cells lacking Not4. In the absence of Not4, Ecm29 interacts less well with the proteasome and becomes ubiquitinated and degraded. Our results characterize Ecm29 as a proteasome chaperone whose appropriate interaction with the proteasome requires Not4. 

Retracted: No

PubPeer comments:
 Figure 2A. * Blue boxes: The E2F6 and E2F1 panels appear to look very similar to each other, while the plots in Figure 2B differ. Could the authors please clarify if these panels are supposed to look so similar? ![file] , 
 2021 correction. https: jvi.asm.org content 95 4 e02197-20 Volume 94, no. 22, e01209-20, 2020, https: doi.org 10.1128 JVI.01209-20 . Page 5, Fig. 2A: Due to an error in figure assembly, the E2F1 panel was an inadvertent duplicate of the E2F6 panel. The E2F1 panel of Fig. 2A should appear as shown below. ,
Protein-energy malnutrition decreases the expression of TLR-4/MD-2 and CD14 receptors in peritoneal macrophages and reduces the synthesis of TNF-alpha in response to lipopolysaccharide (LPS) in mice
Authors: Luiz Carlos de Sá Rocha
Ricardo Ambrósio Fock
Vanessa de Moura Sá Rocha
Primavera Borelli
Marco Aurélio Ramirez Vinolo
Journal: Cytokine (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Protein-energy malnutrition; Inflammatory response; LPS; TNF-alpha; IL-1alpha
Affiliations: Experimental Haematology Laboratory, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of São Paulo, Brazil.

Abstract:  Protein-energy malnutrition (PEM) modifies resistance to infection, impairing a number of physiological processes, including hematopoiesis. In this study, we examined a few aspects of the inflammatory response to LPS in a model of PEM. We evaluated the cellularity of the blood, bone marrow and spleen, as well as phagocytic, fungicidal and spreading activity, the production in vivo and in vitro of TNF-alpha, IL-1alpha and IL-6, and the expression of CD14 and TLR-4/MD-2 receptors in macrophages. Two-month-old male Swiss mice were submitted to PEM with a low-protein diet containing 4% protein as compared to 20% protein in the control diet. When the experimental group had attained about 20% loss of their original body weight, they were used in the experiments. Malnourished animals presented anemia, leucopenia and severe reduction in bone marrow, spleen and peritoneal cavity cellularity. The production of TNF-alpha, IL-1alpha and IL-6 stimulated in vivo with LPS and the production of IL-6 in bone marrow cells cultured with LPS and the production of TNF-alpha in bone marrow, spleen and peritoneal cells cultured with LPS were significantly lower in malnourished animals. The expression of CD14 and TLR-4/MD-2 receptors was found to be significantly lower in macrophages of malnourished animals. These findings suggest that malnourished animals present a deficient response to LPS. The lower expression of the CD14 and TLR-4/MD-2 receptors may be partly responsible for the immunodeficiency observed in the malnourished mice. These data lead us to infer that the nutritional state interferes with the activation of macrophages and with the capacity to mount an immune response. 

Retracted: No

PubPeer comments:
 Figure 5. More similar than expected. Could authors check, please? ![file] ,
Pannexin 3 inhibits proliferation of osteoprogenitor cells by regulating Wnt and p21 signaling
Authors: Yoshihiko Yamada
Satoshi Fukumoto
Masaki Ishikawa
Tsutomu Iwamoto
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ATP; Calcium Intracellular Release; Cell Proliferation; Hemichannel and ER Ca2+ Channel; Intracellular ATP and Ca2+ levels
Affiliations: From the Laboratory of Cell and Developmental Biology, NIDCR, National Institutes of Health, Bethesda, Maryland 20892-4370.

Abstract:  Canonical Wnt signaling and BMP promote the proliferation and differentiation of osteoprogenitors, respectively. However, the regulatory mechanism involved in the transition from proliferation to differentiation is unclear. Here, we show that Panx3 (pannexin 3) plays a key role in this transition by inhibiting the proliferation and promoting the cell cycle exit. Using primary calvarial cells and explants, C3H10T1/2 cells, and C2C12 cells, we found that Panx3 expression inhibited cell growth, whereas the inhibition of endogenous Panx3 expression increased it. We also found that the Panx3 hemichannel inhibited cell growth by promoting β-catenin degradation through GSK3β activation. Additionally, the Panx3 hemichannel inhibited cyclin D1 transcription and Rb phosphorylation through reduced cAMP/PKA/CREB signaling. Furthermore, the Panx3 endoplasmic reticulum Ca(2+) channel induced the transcription and phosphorylation of p21, through the calmodulin/Smad pathway, and resulted in the cell cycle exit. Our results reveal that Panx3 is a new regulator that promotes the switch from proliferation to differentiation of osteoprogenitors via multiple Panx3 signaling pathways. 

Retracted: No

PubPeer comments:
 The immunoblot for Tubulin appear to look similar in red boxes in Fig 6A and Fig 7A. ![file] ,
MiR-29 regulates retinopathy in diabetic mice via the AMPK signaling pathway
Authors: B-W Zhao
Y-W Liu
H-Y Dai
L-N Hao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-29; retinopathy; diabetic mice; AMPK signaling pathway; electroretinogram
Affiliations: Department of Ophthalmology, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang, China. .

Abstract:  Objective: This work aims to study the influence of micro-ribonucleic acid (miR)-29 on the retinopathy in diabetic mice via the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway. Materials and methods: A total of 24 C57BL/6 mice were randomly divided into normal group (n=12) and model group (n=12). Mice in the normal group were given to normal diet, and those in the model group were prepared for establishing diabetes mouse model. After animal procedures, electroretinogram was performed to detect the latent period and amplitude of b-wave. The expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected via immunohistochemistry. The protein levels of the phosphorylated AMPK (p-AMPK) and phosphorylated mammalian target of rapamycin (p-mTOR) were determined using Western blotting. Moreover, miR-29 expression and cell apoptosis were detected via quantitative Polymerase Chain Reaction (qPCR) and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL), respectively. Results: Compared with those in the normal group, the latent period prolonged and amplitude of b-wave decreased in the model group (p&lt;0.05). Immunohistochemistry showed that compared with normal group, mice in the model group exhibited increased Bax expression and decreased Bcl-2 expression (p&lt;0.05). The Western blotting analysis showed that the protein levels of p-AMPK decreased and p-mTOR increased in the model group compared with those in the normal group (p&lt;0.05). The qPCR revealed that compared with the normal group, the model group had notably decreased miR-29 expression (p&lt;0.05). TUNEL detection displayed that the apoptotic rate was remarkably elevated in the model group compared with that in the normal group (p&lt;0.05). Conclusions: Inhibition of miR-17-5p up-regulates the expression of VEGF-A and GDNF in MSCs, and promotes the repair of spinal cord injury by MSCs. 

Retracted: No

PubPeer comments:
 Figure 1.  Expressions of Bax and Bcl2 detected via the immunohistochemistry ![file] Bax (Normal group) and Bcl-2 (Model group) appear to be the same. , 
  Figure 3. Protein expressions detected via Western blotting. I have added a 180-deg rotation of the p-AMPK band. ![file] What appear to be the same loading control and the same p-AMPK band can be found in other papers by unrelated authors. Clockwise from upper left: Figure 3 from [Sun et al (2019)] .  NF-u03baB protein expression determined through Western blotting ; Fig 3 from [Long et al (2019)] ; Fig 4 from [Lou et al (2019)] ; and Figure 5 from [Pan et al (2019)] . ![] ,
Alpha-enolase as a potential cancer prognostic marker promotes cell growth, migration, and invasion in glioma
Authors: Tianshi Que
Xi&#x27;an Zhang
Gang Wang
Hao Long
Zhiyong Li
Zhen Liu
Zheng Hu
Liu Yi
WeiYi Fang
Ye Song
Songtao Qi
Qisheng Luo
Journal: Molecular Cancer (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: glycolytic inhibitors; alpha-enolase (ENO1); tumor progression; prognosis; glioma
Affiliations: Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China. .

Abstract:  Background: The success of using glycolytic inhibitors for cancer treatment relies on better understanding the roles of each frequently deregulated glycolytic genes in cancer. This report analyzed the involvement of a key glycolytic enzyme, alpha-enolase (ENO1), in tumor progression and prognosis of human glioma. Methods: ENO1 expression levels were examined in glioma tissues and normal brain (NB) tissues. The molecular mechanisms of ENO1 expression and its effects on cell growth, migration and invasion were also explored by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, Transwell chamber assay, Boyden chamber assay, Western blot and in vivo tumorigenesis in nude mice. Results: ENO1 mRNA and protein levels were upregulated in glioma tissues compared to NB. In addition, increased ENO1 was associated disease progression in glioma samples. Knocking down ENO1 expression not only significantly decreased cell proliferation, but also markedly inhibited cell migration and invasion as well as in vivo tumorigenesis. Mechanistic analyses revealed that Cyclin D1, Cyclin E1, pRb, and NF-κB were downregulated after stable ENO1 knockdown in glioma U251 and U87 cells. Conversely, knockdown of ENO1 resulted in restoration of E-cadherin expression and suppression of mesenchymal cell markers, such as Vimentin, Snail, N-Cadherin, β-Catenin and Slug. Furthermore, ENO1 suppression inactivated PI3K/Akt pathway regulating the cell growth and epithelial-mesenchymal transition (EMT) progression. Conclusion: Overexpression of ENO1 is associated with glioma progression. Knockdown of ENO1 expression led to suppressed cell growth, migration and invasion progression by inactivating the PI3K/Akt pathway in glioma cells. 

Retracted: No

PubPeer comments:
 https: twitter.com EikoFried status 1380630175264673795 ,
Phosphatidylethanolamine, a limiting factor of autophagy in yeast strains bearing a defect in the carboxypeptidase Y pathway of vacuolar targeting
Authors: Sabine Rosenberger
Ruth Nebauer
Günther Daum
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Vps4p; Vps36p; Saccharomyces cerevisiae; vacuole; carboxypeptidase Y pathway

Abstract:  Vps4p and Vps36p of Saccharomyces cerevisiae are involved in the transport of proteins to the vacuole via the carboxypeptidase Y pathway. We found that deletion of VPS4 and VPS36 caused impaired maturation of the vacuolar proaminopeptidase I (pAPI) via autophagy or the cytosol to vacuole targeting pathway. Supplementation with ethanolamine rescued this defect, leading to an increase of the cellular amount of phosphatidylethanolamine (PtdEtn), an enhanced level of the PtdEtn-binding autophagy protein Atg8p and a balanced rate of autophagy. We also discovered that maturation of pAPI was generally affected by PtdEtn depletion in a psd1Delta psd2Delta mutant due to reduced recruitment of Atg8p to the preautophagosomal structure. Ethanolamine supplementation provided the necessary amounts of PtdEtn for complete maturation of pAPI. Since the expression level of Atg8p was not compromised in the psd1Delta psd2Delta strain, we concluded that the amount of available PtdEtn was limiting. Thus, PtdEtn appears to be a limiting factor for the balance of the carboxypeptidase Y pathway and autophagy/the cytosol to vacuole targeting pathway in the yeast. 

Retracted: No

PubPeer comments:
 Left: Figure 1.  u03b17nAchR agonist pretreatment alleviates pathological injury in the hippocampus. Hippocampal tissues were examined at T3 by hematoxylin eosin staining to evaluate the protective effects of u03b17nAchR agonist. **The hippocampal samples collected from the (A) Sham control group exhibited no evidence of morphological damage**, whereas (B) hippocampal tissues of the rats with CPB model group exhibited signs of obvious cellular degeneration and abnormal cell arrangements. **(C) Rats pretreated with u03b17nAchR agonist prior to CPB surgery exhibited only slight morphological alterations compared with the CPB group**; however, more obvious pathological changes were observed in rats (D) cou2011treated with the u03b17nAchR antagonist. Right: Fig. 2A from [Chen et al (2017)] - 4 mL kg panel.  Different concentrations of HRS attenuated brain tissue injury after CPB. After establishment of the rat CPB model, animals were treated with 1 mL kg, **4 mL kg**, or 6 mL kg of HRS. At 24 h after CPB, the hippocampus was stained with HE to assess pathological changes. ... A: HE staining . ![file] Overlaps marked. , 
 Figure 3.  u03b17nAchR agonist pretreatment inhibits Caspase 3 protein expression in the hippocampus.... (C) Immunohistochemistry for Caspase 3 in hippocampus at T2. Magnification, x400; scale bar, 20 u00b5m; red arrows indicate positive expressions . ![file] Compare with Fig. 4 from [Chen et al (2017)] .  HRS inhibited neuronal apoptosis via the PI3K Akt GSK3u03b2 signaling pathway after CPB in rats. ![file] ,
Comparison of invasion of fibroblasts and macrophages by high- and low-virulence Leptospira strains: colonization of the host-cell nucleus and induction of necrosis by the virulent strain
Authors: Jie Yan
Liwei Li
David M Ojcius
Journal: Archives of microbiology (2007)
Discipline: MICROBIOLOGY
Keywords: Leptospira interrogans; high-virulence; low-virulence; fibroblasts; macrophages
Affiliations: Department of Medical Microbiology and Parasitology, Medical School of Zhejiang University, Hangzhou, 310058 China.

Abstract:  The infection cycle of low- and high-virulence strains of Leptospira interrogans was compared in fibroblasts and macrophages. L. interrogans serovar Lai strain Lai was used as a representative high-virulence strain, while L. interrogans serovars Pomona strain Luo was used as a low-virulence strain. L. biflexa serovar Patoc strain Patoc I, a nonparasitic strain of Leptospira, was used as a control. Both the high- and low-virulence strains could adhere to fibroblasts and macrophages using one or both ends of the spirochete, which was followed by phagocytosis of both strains. Both strains adhered more strongly to macrophages than fibroblasts. However, the high-virulence strain could invade the host-cell nucleus, while the low-virulence strain remained in phagosomes. The L. biflexa strain neither adhered to nor invaded either cell type. Both of the L. interrogans strains also induced cell death (mostly necrosis) of macrophages, whether or not the spirochetes were viable, suggesting that leptospiral virulence is unrelated to macrophage death. However, the high-virulence strain induced mainly necrosis in fibroblasts, while the low-virulence strain induced more apoptosis. Thus, the main feature distinguishing the two L. interrogans strains is the ability of the high-virulence strain to invade the host-cell nucleus and induce pro-inflammatory necrosis in fibroblasts. 

Retracted: No

PubPeer comments:
 Authors from the same lab seemed reuse their images between papers. The same reused images did seem represent the same experimental condition. However, it is expected that the authors acknowledge the images were used previously in other of their publications. The other paper ([Liu, et al 2007] ) is flagged in a different thread. ![] ![] , 
 Found another duplication between them, although there are two spots different. ![file] ![file] ,
Investigation of the effect of pomegranate extract and monodisperse silver nanoparticle combination on MCF-7 cell line
Authors: Birgütay Şahin
Hülya Gündüz
Enes Demir
Fatih Şen
Ayşenur Aygün
Journal: Journal of Biotechnology (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cytotoxicity; Green synthesis; MCF-7; Nanomaterials; Silver nanoparticles.
Affiliations: Sen Research Group, Department of Biochemistry, University of Dumlupınar, 43000 Kütahya, Turkey., Sen Research Group, Department of Biochemistry, University of Dumlupınar, 43000 Kütahya, Turkey. Electronic address: .

Abstract:  In this study, we aimed to investigate whether the combination therapy of pomegranate extract and silver nanoparticle is effective on MCF-7 cell culture. The pomegranate extract was mixed and incubated with silver nitrate for the microwave assisted green synthesized of silver nanoparticle. Obtained nanoparticles were investigated using X-ray diffraction (XRD), Fourier Transform Infrared Spectroscopy (FTIR), UV-vis, Field Emission Scanning Electron Microscopy (FESEM), and Transmission Electron Microscopy (TEM) methods The spectroscopic and morphological studies of the monodisperse Ag NPs which have particle size of 15.4nm indicate the highly crystalline form, well dispersity, and colloidally stable NPs. After fully characterization of prepared nanoparticles, the effectiveness of Ag NPs was determined by evaluating cell viability, nuclear degradation and cell cycle parameters. The results obtained demonstrate that biosynthesized Ag NPs can inhibit the proliferation of human breast cancer cell line MCF-7 in the IC50 at a dose of 12.85μg/mL and inhibit the proliferation of Ag NPs against anti-growth arresting MCF-7 cell line. This case demonstrates that it may exert its proliferative effect by reducing DNA synthesis and apoptosis-inducing cell cycle stages. 

Retracted: No

PubPeer comments:
 Figure 4, panels D E are identical, just two different magnifications. ![file] , 
 Thanks for pointing out the error in the representative images of the comet assay which have no bearing on the outcome of the article. We have already written to the Editor for publishing an Erratum. ,
Long non-coding RNA DDX11-AS1 facilitates gastric cancer progression by regulating miR-873-5p/SPC18 axis
Authors: Xiaochun Liu
Zheng Ren
Yaoran Si
Desheng Yang
Journal: Artificial Cells Nanomedicine and Biotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DDX11-AS1; SEC11A/SPC18; gastric cancer; miR-873-5p.
Affiliations: Department of Digestive Diseases, Henan University Huaihe Hospital, Kaifeng, China, Department of Respiratory Medicine, Henan University Huaihe Hospital, Kaifeng, China

Abstract:  Gastric cancer (GC) is a malignant tumour with high lethality. Accruing evidence elucidates the critical adjusting role of long non-coding RNA (lncRNAs) in human cancers. DDX11 antisense RNA 1 (DDX11-AS1) was previously found to be involved in GC pathogenesis. However, the precise molecular mechanisms of DDX11-AS1 need to be further investigated. In this study, we found that DDX11-AS1 expression was up-regulated in GC tumour tissues and cells. Increased DDX11-AS1 expression was associated with advanced TNM stage and lymph node metastasis. Functionally, knockdown of DDX11-AS1 repressed cell proliferation and clone formation, while induced cell cycle arrest and apoptosis. As expected, DDX11-AS1 overexpression displayed the opposite effect. Mechanically, DDX11-AS1 enhanced SPC18 expression through acting as a ceRNA for miR-873-5p. Furthermore, the inhibitory effect of DDX11-AS1 silencing on malignant biological behaviour of GC cells was attenuated by either miR-873-5p inhibitor or SEC11A up-regulation. Moreover, suppression of DDX11-AS1 also decreased GC tumorigenesis in vivo. In conclusion, DDX11-AS1 may serve as an oncogene in GC progression by sponging miR-873-5p and promoting SPC18 expression, providing a new insight into the mechanisms of DDX11-AS1 and elucidating a promising therapy target in GC. 

Retracted: No

PubPeer comments:
 Fig 2F. I have concerns. ![file] ,
Galphaz inhibits serum response factor-dependent transcription by inhibiting Rho signaling
Authors: Parmesh Dutt
Alan Hall
Keith D Merdek
Aron B Jaffe
Deniz Toksoz
Journal: Molecular pharmacology (2004)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Galpha12/13; Galphaq; Rho GTPase; serum response factor (SRF); gene transcription
Affiliations: Physiology Department, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.

Abstract:  Galpha12/13 or Galphaq signals induce activation of Rho GTPase, leading to serum response factor (SRF)-mediated gene transcription and actin cytoskeletal organization; however, less is known regarding how Rho pathway signals are down-regulated. Here we report that Galphaz signals inhibit serum response factor (SRF)-dependent transcription. Galphaz expression inhibits Galpha12/13-, Galphaq-, and Rho guanine nucleotide exchange factor (GEF)-induced serum response element (SRE) reporter activation in human embryonic kidney 293T and PC-12 cells. Expression of Galphaz mutants with defective fatty acylation has no inhibitory effect. Expression of Galphaz, but not Galphai, attenuates serum-induced SRE reporter activation, suggesting that Galphaz can down-regulate endogenous signals leading to SRF. Whereas Galphaz also blocks SRE reporter induction by the activated mutant RhoAL63, it does not affect Galpha12- or Rho GEF-induced RhoA activation or RhoAL63-GTP binding in vivo. Moreover, Galphaz does not inhibit SRE reporter induction by an activated form of Rho kinase. Because Galphaz inhibits RhoAL63/A188-induced reporter activation, phosphorylation of RhoA on serine 188 does not seem to be involved; furthermore, RhoA subcellular localization was not affected. Use of pharmacologic inhibitors implies that Galphaz-induced reduction of SRE reporter activation occurs via a mechanism other than adenylate cyclase modulation. These findings suggest that Galphaz signals may attenuate Rho-induced stimulation of SRF-mediated transcription. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than expected. ![file] ,
Propofol suppresses proliferation, migration and invasion of gastric cancer cells via regulating miR-29/MMP-2 axis
Authors: Y-J Ni
J Lu
H-M Zhou
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Propofol; gastric cancer; miR-29; MMP-2; proliferation
Affiliations: Department of Anesthesiology, The Second Affiliated Hospital of Jiaxing College, Zhejiang, Jiaxing, China. .

Abstract:  Objective: Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent. Previous studies suggested that propofol might act as anti-tumor drug in various cancers, including gastric cancer. However, the underlying mechanism is still largely unknown. Materials and methods: 1, 5, 10 and 20 μg/ml of propofol were used to treat gastric cancer cell MKN45 for 24, 48 or 72 hours. MTT assay was used to detect the proliferation. Transwell assay was employed to measure the invasion and migration with or without matrigel. The expression of miR-29a, 29b and 29c was assessed by quantitative real time polymerase chain reaction (qRT-PCR). Luciferase assay was introduced to confirm the relationship between miR-29 family member and MMP-2. Western blot was adopted to measure the expression of MMP-2 protein. Results: The proliferation, migration and invasion of gastric cancer cell MKN45 were gradually decreased after propofol treatment in time- and dose- dependent manners. MiR-29a, b and c were downregulated in MKN45 cells compared with normal gastric mucosa epithelial cell GES-1 and upregulated by propofol. Inhibition of miR-29a, b or c promoted cell proliferation, migration and invasion of MKN45 cells under propofol treatment. MMP-2 was a target and regulated by miR-29 family and propofol. MMP-2 silencing reversed the stimulative effects of miR-29 inhibitor. Conclusions: Propofol inhibited cell proliferation, migration and invasion by upregulating miR-29a, miR-29b and miR-29c and downregulating MMP-2. 

Retracted: Yes

PubPeer comments:
 Withdrawn. The journal does not provide any details beyond  This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. The original paper PDF has been removed from the journal s website. , 
 #1 Links may have been removed but the PDF is still on the website: https: www.europeanreview.org wp wp-content uploads 8606-8615.pdf ,
Association of variant on the promoter of cluster of differentiation 74 in graves disease and graves ophthalmopathy
Authors: Yu-Huei Liu
Fuu-Jen Tsai
Chiou-Yuan Shen
Journal: Bioscience reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cluster of differentiation 74; Graves disease; Graves ophthalmopathy; Immunology & Inflammation; Molecular Bases of Health & Disease
Affiliations: Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan., Drug development center, China Medical University, Taichung, Taiwan., Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan., Department of Pediatrics, China Medical University Hospital, Taichung, Taiwan., School of Chinese Medicine, China Medical University, Taichung, Taiwan.

Abstract:  The macrophage migration inhibitory factor (MIF)/cluster of differentiation 74 (CD74) plays a role in immunological functions. The present study aims to investigate whether single-nucleotide polymorphisms (SNPs) in the MIF and CD74 are risk factors for developing Graves ophthalmopathy (GO) in patients with Graves disease (GD). A case-control study enrolled 484 patients with GD (203 with and 281 without GO) and 1000 healthy individuals. SNPs were discriminated using real-time polymerase chain reaction. Hardy-Weinberg equilibrium, as well as frequencies of allele and genotype between GD patients with and without GO, were estimated using the Chi-square test. The effects of CD74 on adipocyte proliferation and differentiation were evaluated using 3T3-L1 preadipocytes. Quantitative DNA-immunoprecipitation was used to detect the binding capacity of NR3C1 and FOXP3 to A/G oligonucleotides. The results showed that individuals carrying the GG genotype at rs2569103 in the CD74 had a decreased risk of developing GD (P=3.390 × 10-11, odds ratio (OR) = 0.021, 95% confidence interval (CI) = 0.003-0.154); however, patients with GD carrying the AG genotype at rs2569103 in the CD74 had an increased risk of developing GO (P=0.009, OR = 1.707, 95% CI = 1.168-2.495). The knockdown of CD74 reduced adipocyte proliferation and differentiation. NR3C1 had a higher affinity for A, whereas FOXP3 had a higher affinity for G of rs2569103. The results suggested the existence of a link between the genetic variation of CD74 promoter and the risk for developing GD and GO, which should be considered in clinical practice. 

Retracted: No

PubPeer comments:
 Figure 4A,C: The flow data presented in Figure 4A and 4C are identical. Figure 3A and 5C: Three micrograph panels have been duplicated and presented as something else. ![file] , 
 I am the first author of this article. Thank you very much for pointing out the mistake. I m sorry that I pasted the wrong image because of my careless editing. I have contacted the magazine to correct these errors. Thank you again for your attention to our research. , 
 #2 Figure 5F also appears to have some issues. Careless editing doesnu2019t seem to apply here. I did not look elsewhere. Cleaved Caspase 3 and 5 appear to be the same image, after flipping vertically. *** ![file] *** Closeup, inverse image and flipped ![file] ,
Radiolabeled PLGA Nanoparticles for Effective Targeting of Bendamustine in Tumor Bearing Mice
Authors: Avinash Gothwal
Ankur Kaul
Anil Kumar Mishra
Umesh Gupta
Iliyas Khan
Rashi Mathur
Journal: Pharmaceutical Research (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PLGA; THP-1; bendamustine; eat; nanoparticles.
Affiliations: Department of Pharmacy, School of Chemical Sciences and Pharmacy, Central University of Rajasthan, Bandarsindri, Ajmer, Rajasthan, 305817, India., Division of Cyclotron and Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, New Delhi, 110054, India., Department of Pharmacy, School of Chemical Sciences and Pharmacy, Central University of Rajasthan, Bandarsindri, Ajmer, Rajasthan, 305817, India. .

Abstract:  Purpose: Bendamustine is an important drug for the treatment of chronic lymphatic leukaemia (CLL), non-Hodgkin lymphoma (NHL). However, its delivery is challenging due to its instability. Current approach reports the development and characterization of bendamustine encapsulated PLGA nanoparticles for the effective targeting to leukemic cells. Methods: The prepared, bendamustine loaded PLGA nanoparticles (BLPNP) were developed and characterized for particle size, zeta potential and polydispersity index. The formed nanoparticles were further characterized with the help of electron microscopy for surface morphology. The formed nanoparticles were evaluated for cytotoxicity, cell uptake, ROS and cell apoptosis against THP-1 leukemic cells as a part of in vitro evaluation. In vivo organ bio-distribution and tumor regression studies were performed to track in vivo behaviour of BLPNP. Results: The average particle size was 138.52 ± 3.25 nm, with 0.192 ± 0.036 PDI and - 25.4 ± 1.38 mV zeta potential. TEM images revealed the homogeneous particle size distribution with uniform shape. In vitro release exhibited a sustained drug-release behaviour up to 24 h. Cytotoxicity against THP-1 cells through MTT assay observed IC50 value of 27.8 ± 2.1 μM for BLPNP compared to pure drug, which was 50.42 ± 3.4 μM. Moreover, in vitro studies like cell-uptake and cell apoptosis studies further confirmed the higher accumulation of BLPNP in comparison to the pure drug. Organ distribution and tumor regression studies were performed to track in vivo behaviour of bendamustine loaded nanoparticles. Conclusion: The overall study described a promising approach in terms of safety, least erythrocytic toxicity, better IC50 value with enhance tumor targeting and regression. 

Retracted: No

PubPeer comments:
 Correction to: Pharm Res https: doi.org 10.1007 s11095-018-2482-6 The typesetter did not use the Fig. 6 provided by the author with his proof corrections, and instead duplicated Fig. 7 by the Fig. 6 caption. The original article has been corrected. ,
Noncanonical autophagy promotes the visual cycle
Authors: Teresa Ann Doggett
Zsolt Ablonczy
Zhenqing Zhou
Alexander V Kolesnikov
Peter H Tang
Douglas R Green
Thomas A Ferguson
Ji-Young Kim
Jennifer Martinez
Chi-Chao Chan
Hui Zhao
Journal: Cell (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Phagocytosis; degradation; photoreceptor outer segments; retinal pigment epithelium; autophagy
Affiliations: Department of Ophthalmology and Visual Sciences, Washington University, St. Louis School of Medicine, St. Louis, MO 63110, USA.

Abstract:  Phagocytosis and degradation of photoreceptor outer segments (POS) by retinal pigment epithelium (RPE) is fundamental to vision. Autophagy is also responsible for bulk degradation of cellular components, but its role in POS degradation is not well understood. We report that the morning burst of RPE phagocytosis coincided with the enzymatic conversion of autophagy protein LC3 to its lipidated form. LC3 associated with single-membrane phagosomes containing engulfed POS in an Atg5-dependent manner that required Beclin1, but not the autophagy preinitiation complex. The importance of this process was verified in mice with Atg5-deficient RPE cells that showed evidence of disrupted lysosomal processing. These mice also exhibited decreased photoreceptor responses to light stimuli and decreased chromophore levels that were restored with exogenous retinoid supplementation. These results establish that the interplay of phagocytosis and autophagy within the RPE is required for both POS degradation and the maintenance of retinoid levels to support vision. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] ,
Rad51 inhibition is an effective means of targeting DNA repair in glioma models and CD133+ tumor-derived cells
Authors: Ka Ian Lio
Maya Shaked-Rabi
Sara Bourne
Susan C Short
Silvia Giampieri
George Sioftanos
Christine Martindale
Mulugeta Worku
Marisa Alcaide-German
Journal: Neuro-Oncology (2011)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: High grade gliomas; Rad51-dependent repair; radiosensitivity; temozolomide; chemo- and radiosensitization
Affiliations: UCL Cancer Institute, University College London, London, UK. 

Abstract:  High grade gliomas (HGGs) are characterized by resistance to radiotherapy and chemotherapy. Targeting Rad51-dependent homologous recombination repair may be an effective target for chemo- and radiosensitization. In this study we assessed the role of Rad51-dependent repair on sensitivity to radiation and temozolomide (TMZ) as single agents or in combination. Repair protein levels in established glioma cell lines, early passage glioblastoma multiforme (GBM) cell lines, and normal human astrocytes (NHAs) were measured using western blot. Viability and clonogenic survival assays were used to measure the effects of Rad51 knockdown with radiation (XR) and TMZ. Immunocytochemistry was used to evaluate kinetics of Rad51 and γ-H2AX repair foci. Immunohistochemistry was used to assess Rad51 protein levels in glioma specimens. Repair proteins including Rad51 are upregulated in HGG cells compared with NHA. Established glioma cell lines show a dose-dependent increase in Rad51 foci formation after XR and TMZ. Rad51 levels are inversely correlated with radiosensitivity, and downregulation markedly increases the cytotoxicity of TMZ. Rad51 knockdown also promotes more residual γ-H2AX foci 24 h after combined treatment. Newly established GBM cell lines also have high Rad51 levels and are extremely sensitive to Rad51 knockdown. Clinical samples from recently resected gliomas of varying grades demonstrate that Rad51 levels do not correlate with tumor grade. Rad51-dependent repair makes a significant contribution to DNA repair in glioma cells and contributes to resistance to both XR and TMZ. Agents targeting Rad51-dependent repair would be effective adjuvants in standard combination regimens. 

Retracted: No

PubPeer comments:
 Figure 1A. Splicing in Rad51 panel, but not in other panels. ![file] ,
Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides
Authors: Srinivas G Mathur
Subrata Sinha
Tapasya Srivastava
Parthaprasad Chattopadhyay
Preeti Shah
Kamal Datta
Journal: Cancer gene therapy (2004)
Discipline: CLINICAL MEDICINE
Keywords: gene therapy; p53; mutant gene; chemotherapy resistance; glioma cells
Affiliations: Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029.

Abstract:  Most gene therapy strategies related to p53 concentrate on the restoration of the activity of mutant p53, as several observations indicate that tumors and cell lines having the mutant gene are resistant to chemotherapy. However, as there is also some evidence to the contrary, we studied the relationship of the p53 status to the cellular response of glioma cells that were exposed to cisplatin. At a concentration of 2.5 microg/ml (which is about half the peak pharmacological blood level reached during chemotherapy), U373MG glioma cells, which had a mutant p53 gene, were more sensitive to the drug as compared to U87MG glioma cells (with normal p53). The U373MG cells responded with apoptosis while U87MG cells responded with a G2-M arrest. In U87MG cells, blocking the p53 response by antisense oligonucleotides also sensitized the cells to 2.5 microg/ml cisplatin, and shifted the cellular response from arrest to caspase 3-mediated apoptosis. A sensitive, p53-independent, mechanism for chemotherapy-induced apoptosis suggests that, in some cases, p53 abrogation by gene therapy or small molecule-based strategies could be a viable therapeutic strategy. 

Retracted: No

PubPeer comments:
 ![file] ,