PReD-Bench/PRed-Bench huggingface dataset:
Balamuthia mandrillaris and Acanthamoeba amebic encephalitis with neurotoxoplasmosis coinfection in a patient with advanced HIV infection
Authors: Alicia Hirzel
Paula Pietrucha-Dilanchian
Panthipa Laowansiri
Yvonne Qvarnstrom
Amilcar Castellano-Sanchez
Govinda S Visvesvara
Claudio Tuda
Joseph C Chan
Kenneth R Ratzan
Journal: Journal of Clinical Microbiology (2012)
Discipline: MICROBIOLOGY
Keywords: HIV infection; Balamuthia mandrillaris; Acanthamoeba amebic encephalitis; Toxoplasma gondii; coinfection
Affiliations: Division of Infectious Diseases, Jackson Memorial Hospital, University of Miami, Miami, Florida, USA. 

Abstract:  We describe a patient with advanced HIV infection and Balamuthia mandrillaris and Acanthamoeba amebic encephalitis with Toxoplasma gondii coinfection. A multidisciplinary effort and state-of-the-art diagnostic techniques were required for diagnosis. Our patient is the first reported case of an HIV-infected person with dual Balamuthia mandrillaris and Acanthamoeba amebic encephalitis with neurotoxoplasmosis coinfection. 

Retracted: Yes

PubPeer comments:
 Images D and E in Figure 2 appear to be the same image transformed as illustrated. *** ![file] , 
  This email is to acknowledge that the American Society for Microbiology has received your email. The ASM takes alleged concerns like these seriously. As such, ASM Journals will follow its Ethics Policies and Procedures for handling and responding to these allegations. , 
 Retraction, October 2021: https: journals.asm.org doi 10.1128 JCM.01838-21  In response to questions raised by concerned readers about the integrity of some of the data in this paper, ASM confirmed evidence of image duplication (though resized and rotated) of panels D and E in Figure 2. ASM and JCM raised the concerns with the authors but were unable to reach a satisfactory resolution. Because the integrity of the data presented was compromised, this publication is retracted in its entirety. We apologize to the readers of JCM and regret any inconvenience that this causes. It is interesting and perhaps encouraging to see ASM take a stronger stance on these types of duplication as they did previously. Previously, ASM stated they would not investigate allegations if the paper was over 6 years old. See e.g. https: retractionwatch.com 2017 06 09 journal-wont-look-allegations-papers-six-years-old-public-websites ,
A Large-Scale Analysis of Impact Factor Biased Journal Self-Citations
Authors: Ludo Waltman
Caspar Chorus
Journal: PLoS ONE (2016)
Discipline: Multidisciplinary
Keywords: citation data; impact factor; self-citations; scholarly journals; ratio
Affiliations: Department of Engineering Systems and Services, Delft University of Technology, Delft, The Netherlands., Centre for Science and Technology Studies, Leiden University, Leiden, The Netherlands.

Abstract:  Based on three decades of citation data from across scientific fields of science, we study trends in impact factor biased self-citations of scholarly journals, using a purpose-built and easy to use citation based measure. Our measure is given by the ratio between i) the relative share of journal self-citations to papers published in the last two years, and ii) the relative share of journal self-citations to papers published in preceding years. A ratio higher than one suggests that a journal's impact factor is disproportionally affected (inflated) by self-citations. Using recently reported survey data, we show that there is a relation between high values of our proposed measure and coercive journal self-citation malpractices. We use our measure to perform a large-scale analysis of impact factor biased journal self-citations. Our main empirical result is, that the share of journals for which our measure has a (very) high value has remained stable between the 1980s and the early 2000s, but has since risen strongly in all fields of science. This time span corresponds well with the growing obsession with the impact factor as a journal evaluation measure over the last decade. Taken together, this suggests a trend of increasingly pervasive journal self-citation malpractices, with all due unwanted consequences such as inflated perceived importance of journals and biased journal rankings. 

Retracted: No

PubPeer comments:
 In the supplementary files, with journal IDs ranging from 4 to 21027, there are gaps, for example: 1-3, 5, 7, 17-19, etc. Could the authors please explain what these gaps represent. For example, are these journals with no citations, with zero self-citations, or something else? ,
Preparation of Fe3O4@SiO2@Layered Double Hydroxide Core–Shell Microspheres for Magnetic Separation of Proteins
Authors: Min Wei
Mingfei Shao
Xue Duan
Fanyu Ning
Jingwen Zhao
David G Evans
Journal: Journal of the American Chemical Society (2012)
Discipline: CHEMISTRY
Keywords: Three-component microspheres; Fe(3)O(4); SiO(2); LDH; nanoplatelet
Affiliations: State Key Laboratory of Chemical Resource Engineering, Beijing University of Chemical Technology, Beijing 100029, People's Republic of China.

Abstract:  Three-component microspheres containing an SiO(2)-coated Fe(3)O(4) magnetite core and a layered double hydroxide (LDH) nanoplatelet shell have been synthesized via an in situ growth method. The resulting Fe(3)O(4)@SiO(2)@NiAl-LDH microspheres display three-dimensional core-shell architecture with flowerlike morphology, large surface area (83 m(2)/g), and uniform mesochannels (4.3 nm). The Ni(2+) cations in the NiAl-LDH shell provide docking sites for histidine and the materials exhibit excellent performance in the separation of a histidine (His)-tagged green fluorescent protein, with a binding capacity as high as 239 μg/mg. The microspheres show highly selective adsorption of the His-tagged protein from Escherichia coli lysate, demonstrating their practical applicability. Moreover, the microspheres possess superparamagnetism and high saturation magnetization (36.8 emu/g), which allows them to be easily separated from solution by means of an external magnetic field and subsequently reused. The high stability and selectivity of the Fe(3)O(4)@SiO(2)@NiAl-LDH microspheres for the His-tagged protein were retained over several separation cycles. Therefore, this work provides a promising approach for the design and synthesis of multifunctional LDH microspheres, which can be used for the practical purification of recombinant proteins, as well as having other potential applications in a variety of biomedical fields including drug delivery and biosensors. 

Retracted: No

PubPeer comments:
 Authors are informed here that their Figure S4 B showing  Fe3O4@NiAl-LDH microspheres synthesized without a SiO2 layer in supporting information file is identical to Figure 4 C showing  Fe3O4@NiO hierarchical microspheres in different paper published one year later: https: pubpeer.com publications 732D32C317D8EC5DF596A37EDDD5BD# DOI: 10.1039 c2ra22495j Two papers seem to have different authors and different affiliations. ![file] , 
 Image of Fe3O4@SiO2@ZnAl-LDH in supporting information (Figure S3) shows unexpected similarity to Figure 1 B (SiO2 NiAl-LDH coreu2212shell microspheres) in: https: pubpeer.com publications FB44B5B1E063D25DE904DA069F0EE6# ![file] ,
MEG3 overexpression inhibits the tumorigenesis of breast cancer by downregulating miR-21 through the PI3K/Akt pathway
Authors: Xinguang Qiu
Xiaochun Wang
Mingzhi Zhu
Lin Li
Yuanting Gu
Fang Wang
Journal: Archives of Biochemistry and Biophysics (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Breast cancer; Glycolysis; MEG3; The PI3K/Akt pathway; miR-21.
Affiliations: Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China., Department of Breast Surgery, Affiliated Hospital of Hebei University, Baoding, 071000, China., Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. Electronic address: .

Abstract:  Increasing studies have highlighted the critical role of lncRNAs in cancer pathogenesis and development. LncRNA maternally expressed gene 3 (MEG3) was reported to function as a tumor suppressor in breast cancer. However, the detailed molecular mechanism of MEG3 involved in breast cancer progression remains far from being addressed. Our findings showed that MEG3 was downregulated and miR-21 was upregulated in breast cancer patient tissues and cells. MEG3 overexpression suppressed cell proliferation and glycolysis, and induced apoptosis in breast cancer cells. MEG3 was demonstrated to function as a molecular sponge of miR-21 and suppress its expression. Moreover, miR-21 upregulation partially abolished the effects of MEG3 overexpression on cell proliferation, glycolysis, and apoptosis in breast cancer cells. Additionally, enforced expression of MEG3 reversed miR-21-mediated activation of PI3K/Akt pathway in breast cancer cells. In vivo experiment demonstrated that overexpression of MEG3 inhibited tumor growth in breast cancer by suppressing miR-21. In summary, MEG3 overexpression inhibited the tumorigenesis of breast cancer by downregulating miR-21 through the PI3K/Akt pathway. 

Retracted: No

PubPeer comments:
 Fig 2F.  Overexpression of MEG3 inhibited the tumorigenesis of breast cancer cells. MCF-7 and MDA-MB-231 cells were transfected with MEG3 or pcDNA, followed by incubation for the indicated time. ... (F) Flow cytometry analysis was conducted to analyze apoptosis of the transfected MCF-7 and MDA-MB-231 cells. These neatly -delineated bags of Tetris blocks are not really plausible as measurements of cells sampled randomly from underlying distributions. ![file] ,
Stat3 dimerization regulated by reversible acetylation of a single lysine residue
Authors: Zheng-Long Yuan
Devasis Chatterjee
Y Eugene Chin
Ying-Jie Guan
Journal: Science (2005)
Discipline: Multidisciplinary
Keywords: Cytokine treatment; Signal transducers; Activators of transcription; STAT family; Phosphorylated
Affiliations: Department of Surgery, Brown University Medical School-Rhode Island Hospital, Providence, RI 02903, USA.

Abstract:  Upon cytokine treatment, members of the signal transducers and activators of transcription (STAT) family of proteins are phosphorylated on tyrosine and serine sites within the carboxyl-terminal region in cells. We show that in response to cytokine treatment, Stat3 is also acetylated on a single lysine residue, Lys685. Histone acetyltransferase p300-mediated Stat3 acetylation on Lys685 was reversible by type I histone deacetylase (HDAC). Use of a prostate cancer cell line (PC3) that lacks Stat3 and PC3 cells expressing wild-type Stat3 or a Stat3 mutant containing a Lys685-to-Arg substitution revealed that Lys685 acetylation was critical for Stat3 to form stable dimers required for cytokine-stimulated DNA binding and transcriptional regulation, to enhance transcription of cell growth-related genes, and to promote cell cycle progression in response to treatment with oncostatin M. 

Retracted: No

PubPeer comments:
null, 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 #3 ![file] , 
 #4 ![file] , 
 Figure 3C. Much more similar than expected. ![file] ,
GSM 900 MHz radiation inhibits ants' association between food sites and encountered cues
Authors: Marie-Claire Cammaerts
Xavier Patris
Zoheir Rachidi
Philippe De Doncker
François Bellens
David Cammaerts
Journal: Electromagnetic Biology and Medicine (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: kinetics; acquisition; loss; olfactory cues; visual cues
Affiliations: Université Libre de Bruxelles, Faculté des Sciences, Bruxelles, Belgium. 

Abstract:  The kinetics of the acquisition and loss of the use of olfactory and visual cues were previously obtained in six experimental colonies of the ant Myrmica sabuleti meinert 1861, under normal conditions. In the present work, the same experiments were conducted on six other naive identical colonies of M. sabuleti, under electromagnetic radiation similar to those surrounding GSM and communication masts. In this situation, no association between food and either olfactory or visual cues occurred. After a recovery period, the ants were able to make such an association but never reached the expected score. Such ants having acquired a weaker olfactory or visual score and still undergoing olfactory or visual training were again submitted to electromagnetic waves. Not only did they lose all that they had memorized, but also they lost it in a few hours instead of in a few days (as under normal conditions when no longer trained). They kept no visual memory at all (instead of keeping 10% of it as they normally do). The impact of GSM 900 MHz radiation was greater on the visual memory than on the olfactory one. These communication waves may have such a disastrous impact on a wide range of insects using olfactory and/or visual memory, i.e., on bees. 

Retracted: No

PubPeer comments:
 There is some strange math in this article. Silly mistakes that should have been caught by the editors and reviewers like formulas where Pius is used instead of Greek letter $pi$, and to make things worse, the authors write Pius = 22 7 = 3.1416 . But more serious is the problem with the data. The variance between observation moments and between colonies is far below anything you might expect. There is no way these numbers can be right. The previous Editor in Chief (prof. Henry Lai) has been informed about these issues in 2013, but his reply was that he thought  it is a very well carried out research . Either he didn t understand the problems or just chose to ignore them. More info on https: www.pepijnvanerp.nl 2013 02 ants-performing-statistical-miracle-under-gsm-phone-radiation ,
MicroRNA-221 regulates chondrogenic differentiation through promoting proteosomal degradation of slug by targeting Mdm2
Authors: Eun-Jung Jin
Jinsoo Song
Dongkyun Kim
Journal: Journal of Biological Chemistry (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MicroRNAs; chondrogenic differentiation; chick limb mesenchymal cells; miR-221; peanut agglutinin-based antisense oligonucleotides

Abstract:  MicroRNAs (miRNAs) are small RNAs that fulfill diverse functions by negatively regulating gene expression. Here, we investigated the involvement of miRNAs in the chondrogenic differentiation of chick limb mesenchymal cells and found that the expression of miR-221 increased upon chondrogenic inhibition. Blockade of miR-221 via peanut agglutinin-based antisense oligonucleotides reversed the chondro-inhibitory actions of a JNK inhibitor on the proliferation and migration of chondrogenic progenitors as well as the formation of precartilage condensations. We determined that mdm2 is a relevant target of miR-221 during chondrogenesis. miR-221 was necessary and sufficient to down-regulate Mdm2 expression, and this down-modulation of Mdm2 by miR-221 prevented the degradation of (and consequently up-regulated) the Slug protein, which negatively regulates the proliferation of chondroprogenitors. These results indicate that miR-221 contributes to the regulation of cell proliferation by negatively regulating Mdm2 and thereby inhibiting Slug degradation during the chondrogenesis of chick limb mesenchymal cells. 

Retracted: Yes

PubPeer comments:
 2020 retraction. http: www.jbc.org content 295 2 668 This article has been withdrawn by the authors. The control day 4 image in Fig. 1C was reused in Kim, D., et al. (2012) J. Biol. Chem. 287, 12501u201312509. The Sox-9 immunoblot in Fig. 4A was reused in Kim, D., et al. (2012) J. Biol. Chem. 287, 12501u201312509. ,
microRNA‑577 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting homeobox A1
Authors: Dandan Nie
Lan Men
Haiying Nie
Journal: Molecular Medicine Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: miR-577; NSCLC; tumor suppressor; oncogene; HOXA1
Affiliations: Department of Gastrointestinal Medicine, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Jilin Entry‑Exit Inspection and Quarantine Bureau, Changchun, Jilin 130062, P.R. China, Department of Vascular Surgery, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China

Abstract:  An increasing number of studies have indicated that the dysregulation of microRNAs (miRNAs/miR) is closely associated with non‑small cell lung cancer (NSCLC) development and progression by acting as tumor suppressors or oncogenes. Therefore, an in‑depth understanding of the biological roles of miRNAs in NSCLC may provide novel therapeutic methods for the treatment of patients with this disease. In the present study, reverse transcription‑quantitative polymerase chain reaction was used to detect miR‑577 expression in NSCLC tissues and cell lines. Cell Counting Kit‑8 and Transwell invasion assays were performed to determine the effects of miR‑577 on NSCLC cell proliferation and invasion. Luciferase reporter assays were used to demonstrate the relationship between miR‑577 and homeobox A1 (HOXA1) in NSCLC cells. The results revealed that miR‑577 was markedly downregulated in NSCLC tissues and cell lines. Additionally, restoration of miR‑577 expression significantly decreased the proliferation and invasion of NSCLC cells. Furthermore, miR‑577 negatively regulated HOXA1 expression in NSCLC cells by directly binding to its 3'‑untranslated region. HOXA1 was significantly upregulated in NSCLC tissues, and its upregulation was inversely correlated with miR‑577. Notably, restored HOXA1 expression abrogated the reduced proliferation and invasion of NSCLC cells caused by miR‑577 overexpression. Taken together, these results indicated that miR‑577 may have served tumor suppressive roles in NSCLC by directly targeting HOXA1. Therefore, this miRNA may be developed as a potential therapeutic target for the therapy of patients with NSCLC. 

Retracted: No

PubPeer comments:
 Figs 3D, 4B, 5A B. ![file] Surprisingly similar Western Blots, stylised in the same manner, illustrate a corpus of [at least 150 papers] (with 50 so far retracted). Here , for example, Figs 3D, 4A, 5A from [Li et al (2018)] : ![] Figs 3D, 4B, 5A from [Lv, Zheng Huang (2018)] . ![] ,
MicroRNA-30a Targets ATG5 and Attenuates Airway Fibrosis in Asthma by Suppressing Autophagy
Authors: Bin Bin Li
Fuzhen Pang
Yun Long Chen
Journal: Inflammation (2020)
Discipline: IMMUNOLOGY
Keywords: ATG5; Airway fibrosis; Asthma; Autophagy; miR-30a.
Affiliations: Department of Paediatrics, Tiantai County People's Hospital, 1 Kang ling Road, Tiantai County, Taizhou City, Zhejiang, China., Department of Medicine, The Children's Hospital of Hangzhou, 196 Wen Hui Road, Hangzhou, 310014, China. ., Department of Paediatrics, Tiantai County People's Hospital, 1 Kang ling Road, Tiantai County, Taizhou City, Zhejiang, China. .

Abstract:  Asthma is the most common chronic disease of childhood, chronic airway inflammation; bronchial tissue fibrosis, is a pathological feature common to children asthma, and an emerging data has indicted that autophagy plays critical roles in airway inflammation and fibrosis-mediated airway remodeling. The aim of this study was to examine whether the antifibrotic effect of epithelial microRNAs (miRNAs) relies on regulating autophagy-mediated airway remodeling and to identify the factors involved and the underlying mechanisms. Our results showed miR-30a were downregulated in children with asthma and ovalbumin (OVA) mouse model in parallel with the upregulation of autophagy-related proteins; moreover, we observed miR-30a inhibited the autophagy by downregulated autophagy-related 5 (ATG5). Then, we observed that overexpression of miR-30a suppressed the fibrogenesis and autophagic flux which was stimulated by interleukin-33 (IL-33) in bronchial epithelial cells. In vivo experiments showed that miR-30a overexpression decreased airway remodeling by decreased autophagy. This study uncovered a previously unrecognized antifibrotic role of miR-30a in asthma, in IL-33-induced lung epithelial cells in vitro, and in a murine model of OVA-induced airway inflammation in vivo and explored the underlying mechanisms. 

Retracted: No

PubPeer comments:
 In Figure 4f, a micrograph has been duplicated and presented as something else. ![file] ,
MicroRNA-204 silencing relieves pain of cervical spondylotic radiculopathy by targeting GDNF
Authors: Zhi-Shui Zhou
Lu-Ping Pan
Nan-Nan Zhai
Wen-Sheng Shen
Cun-Feng Li
Journal: Gene Therapy (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cervical spondylosis; neuropathic pain; miR-204; GDNF; neuroinflammation
Affiliations: Department of Anesthesiology, Shaoxing Paojiang Hospital, Shaoxing, 312000, PR China. ., Department of Anesthesiology, Shaoxing Hospital of Traditional Chinese Medicine, Shaoxing, 312000, PR China.

Abstract:  Cervical spondylosis may cause chronic neck pain, radiculopathy and/or myelopathy, and consequently results in severe brain damage. Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for motoneurons. Accumulating microRNAs (miRNAs) have highlighted as critical regulators of GDNF signaling in the mediation of neuroinflammation and neuropathic pain. Hence, we performed this study to investigate the potential role of miR-204 in the neuropathic pain of cervical spondylotic radiculopathy (CSR) by targeting GDNF. A rat model of spinal cord compression (SCC) was established to stimulate a pathologic lesion. RT-qPCR and western blot assays characterized the downregulation of GDNF and the upregulation of miR-204 in spinal cord tissues of rats under the conditions of SCC. Moreover, miR-204 could directly target GDNF, as evidenced by dual-luciferase reporter gene assay. In order to elucidate the roles of miR-204 and GDNF in SCC-induced neuropathic pain, miR-204 sponge, GDNF, or shRNA against GDNF was introduced to the rats, followed by measurements for SCC-induced neuroinflammation and neuropathic pain. GDNF upregulation or miR-204 silencing was identified to reduce the spontaneous pain score, gait scores and cell apoptosis. Furthermore, GDNF upregulation or miR-204 silencing resulted in elevated amplitude of sensory-evoked potentials (SEPs), number of motoneurons, release of pro-inflammatory factors, TNF-α, and IL-1β in addition to an increase in the anti-inflammatory factor BDNF. Taken together, upregulation of GDNF induced by miR-204 silencing confers protection against SCC-induced pain in rat models, suggesting a potential therapeutic target for CSR treatment. 

Retracted: No

PubPeer comments:
 Figure 5C: There is an overlap, I ve added the magenta rectangles to show where I mean. Would the authors please comment? ![file] ,
The expression and pharmacological characterization of nicotinic acetylcholine receptor subunits in HBE16 airway epithelial cells
Authors: Juliy M Perelman
Xiangdong Zhou
Qi Li
Victor P Kolosov
Journal: Cell Biochemistry and Biophysics (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: nicotinic acetylcholine receptor; human airway epithelial cells; gene expression; protein expression; inflammatory factors
Affiliations: Division of Respiratory Medicine, Second Affiliated Hospital, Chongqing Medical University, No.74, Linjiang Road, Yuzhong District, Chongqing 400010, China.

Abstract:  This study characterizes the expression and the biological effects of the nicotinic acetylcholine receptor (nAChR) on human airway epithelial cells. Cultured HBE16 airway epithelial cells were incubated with either nicotine or cigarette smoke extract (CSE). The nAChR gene and protein expression in cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, and western blot. The protein expression of the nAChR subunits, α1, α5, and α7, were evaluated by immunohistochemistry. Cells were subsequently transfected with α1-, α5-, and α7-specific siRNAs, and the effects of nicotine on the production of the pro-inflammatory factors, TNF-α, IL-8, and IL-6 in transfected cells were analyzed using an enzyme-linked immunosorbent assay and real-time PCR. We detected α1, α5, α7, and β2 subunits in untreated HBE16 cells, and their expression was elevated after nicotinic incubation. Importantly, the most significant increase in expression was observed in the α5 and α7 subunits. However, CSE did not cause a significant enhancement in the expression of these genes and proteins. Cells pretreated with nicotine prior to lipopolysaccharide (LPS) stimulation exhibited a lower production of TNF-α, IL-8, and IL-6 compared to LPS-treated (only) cells. Cells that were transfected with α7 siRNA and subsequently incubated with nicotine and LPS, exhibited a higher expression of TNF-α, IL-8, and IL-6 compared with non-transfected cells or α1 and α5 siRNA-transfected cells. In α1- and α5-siRNA-transfected cells, the expression of TNF-α, IL-8, and IL-6 showed no significant difference compared with non-transfected cells. Therefore, we concluded that α1, α5, α7, and β2 nAChR subunits are highly expressed in human bronchial epithelial cells (HBE16) after nicotinic incubation and that the α7 subunit is involved in the nicotine-induced inhibitory effect on the production of inflammatory factors. Moreover, α1, α5, and β2 subunits did not play an important role in this process. 

Retracted: No

PubPeer comments:
 Figure 5A, live animal imaging of mice bearing tumors formed from control (PDT) and scaffold derived MDA-MB-231 cells (SDT). It looks as same mouse was imaged twice. Could the authors please clarify? ![file] ,
Study of the UTMD-based delivery system to induce cervical cancer cell apoptosis and inhibit proliferation with shRNA targeting Survivin
Authors: Kun Liang
Feng Yang
Zhi-Yi Chen
Yan Lin
Journal: International Journal of Molecular Sciences (2013)
Discipline: CHEMISTRY
Keywords: Apoptosis induction; shRNA; gene therapy; ultrasound-targeted microbubble destruction (UTMD); cell proliferation
Affiliations: Department of Medical Ultrasound, Key Laboratory for Major Obstetric Diseases of Guangdong Province, the Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, China. .

Abstract:  Apoptosis induction by short hairpin RNA (shRNA) expression vectors could be an efficient and promising strategy for cancer gene therapy. Ultrasound-targeted microbubble destruction (UTMD) is an appealing technique. In this study, we investigated the apoptosis induction and suppression of cell proliferation in vivo transfected by the UTMD-based shRNA delivery system. Nude mice with transplanted tumors of cervical cancer were randomly arranged into three groups: control group, plasmid injection and ultrasound (P + US), P + UTMD group. Expressions of Survivin and proliferating cell nuclear antigen (PCNA), Bcl-2, Bax, Caspase-3, Ki-67, nucleostemin (NS) were investigated by immunohistochemistry. Furthermore, microvessel density (MVD) was detected by CD34 protein expressions and apoptotic index (AI) was measured by TUNEL. As compared with those in the control and P + US groups, protein expressions of PCNA, Ki-67, Bcl-2, Survivin and NS in P + UTMD groups were down-regulated markedly, while those of Bax, Caspase-3 were up-regulated significantly (p &lt; 0.05). MVD decreased significantly, whereas AI increased remarkably (p &lt; 0.05). We suggested that UTMD-based shRNA delivery system could induce apoptosis and inhibit proliferation significantly, without causing any apparently adverse effect, representing a new, promising technology that would be used in the future gene therapy and research. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Long noncoding RNA SNHG12 promotes the progression of cervical cancer via modulating miR-125b/STAT3 axis
Authors: Wen-S Hu
Xue-J Jin
Hua Zhu
Yan Hu
Shi Li
Lu-L Chen
Xiang-J Chen
Ji-S Xue
Rong-Y Ou
Zhi-F Zhang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: cervical cancer; miR-125b; signal transducer and activator of transcription 3 (STAT3); small nucleolar RNA host gene 12 (SNHG12).
Affiliations: Department of Obstetrics and Gynecology, Hangzhou Women's Hospital (Hangzhou Maternity and Child Health Care Hospital), Hangzhou, China., Department of Gastrointestinal Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Obstetrics and Gynecology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Urology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Abstract:  Increasing evidence showed that long noncoding RNAs (lncRNAs) played an important role in the occurrence and development of tumors. To date, lncRNA small nucleolar RNA host gene 12 (SNHG12) has revealed an oncogenic role in various tumors. However, the role of SNHG12 in cervical cancer is still unclear. Therefore, we focused on the biological function and molecular mechanism of SNHG12 in the tumorigenesis of cervical cancer. In this study, the expression of miR-125b was observably downregulated in cervical cancer cells. Meanwhile, the expression of SNHG12 was obviously upregulated in cervical cancer cell lines (HeLa, SiHa, Caski, C4-1, and C33A) compared with the immortalized cervical epithelial cells. The further assay showed that miR-125b was a target of SNHG12 in cervical cancer. Moreover, a negative relationship between miR-125b and SNHG12 was found in cervical cancer. In addition, SNHG12 inhibition restrained the proliferation, migration, and invasion of cervical cancer cells. Meanwhile, miR-125b mimics repressed the expression of signal transducer and activator of transcription 3 (STAT3). The further assay showed that STAT3 was a target of miR-125b in cervical cancer. In addition, sh-STAT3 repressed the migration and invasion of cervical cancer cells. Furthermore, it showed that miR-125b inhibitors reversed STAT3 expression restrained by the reduction of SNHG12 expression. In general, SNHG12 modulated STAT3 by sponging miR-125b in cervical cancer and played an important role in the development of cervical cancer. 

Retracted: No

PubPeer comments:
 In figure1, figure 1b and figure 1e, figure 1c and figure 1d, figure 1f and figure 1g were similar. In figure5, figure 5b and figure 5f, figure 5c 5d 5g 5h were similar. In figure6, figure 6a and figure 6c was similar. These similar pictures are very strange ,
New-found brake calibrates insulin action in β-cells
Authors: Rohit N Kulkarni
Journal: Nature (2021)
Discipline: Multidisciplinary
Keywords: Diabetes; Metabolism.

Abstract: Insulin is produced by pancreatic β-cells. The identification of a regulator of insulin signalling in these cells cements the long-standing idea that this pathway has a key role in β-cell biology. The protein inceptor restrains insulin signalling through endocytosis.

Retracted: No

PubPeer comments:
 There are no conflicts of interests reported in the editorial (and [none declared in a recent] paper) although there could be some ![file] Maybe Dr Kulkarni could also give a statement if there are any ties to the authors of the study he is commenting on? Travel support to [Munich Octoberfest meetings] where he is listed next to the corresponding author? ,
A new mixed-ligand coordination polymer: protective activity on influenza a virus-induced COPD via regulating tlr3 gene expression on alveolar epithelial cells
Authors: Youhui Tu
Xiangwei Zhang
Chao Yang
Journal: Drug Development and Industrial Pharmacy (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: COPD; Coordination polymer; ELISA; RT-PCR; molecular docking.
Affiliations: Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, China, Department of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China, Department of Respiratory and Critical Care Medicine, Wuxi Branch of Ruijin Hospital, Wuxi, China

Abstract:  A new Cu(II) coordination polymer (CP) of [Cu5(µ3-OH)2(bcpt)4(bib)2] (1, bib = 1,4-bis(1-imidazoly)benzene and H2bcpt = 3,5-bis(3'-carboxyphenyl)-1,2,4-triazole) was synthesized by reaction of Cu(NO3)2·3H2O reacting with 3,5-bis(3'-carboxyphenyl)-1,2,4-triazole in the existence of 1,4-bis(1-imidazoly)benzene as the second ligand. The treatment activity of the compound on influenza A virus induced chronic obstructive pulmonary disease (COPD) was evaluated. First, the biological function of the lung was assessed by measuring the partial pressure for the carbon dioxide (PaCO2) and oxygen (PaO2) via the analysis of blood gas. Next, the inflammatory cytokines released by alveolar epithelial cells were determined via the ELISA test kit. In addition to this, the real-time RT-PCR was carried out to determine the inflammatory response relative expression in the alveolar epithelial cells. Finally, the relative expression of the TLR3 on the alveolar epithelial cells was revealed by western blot. Possible binding patterns were acquired from the post scoring software and molecular docking, which exhibited two possible functional side chain binding sites of TLR3 to compounds binding, possibly offering distinct regulatory mechanisms. 

Retracted: No

PubPeer comments:
 In Figure 1, the beads laying in the so called microwell chip do not look like beads, but perfect circles. The size of the microwell chip is not impressive given the presented scale bars... ![file] ,
The proline repeat domain of p53 binds directly to the transcriptional coactivator p300 and allosterically controls DNA-dependent acetylation of p53
Authors: Ted R Hupp
Lindsay Burch
David Dornan
Amanda J Smith
Harumi Shimizu
Journal: Molecular and Cellular Biology (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p300; acetylation; p53; conformational constraints; DNA
Affiliations: Cancer Research UK Laboratories, P53 Signal Transduction Group, Department of Molecular and Cellular Pathology, University of Dundee, Dundee DD1 9SY, United Kingdom., Cancer Research UK Laboratories, P53 Signal Transduction Group, Department of Molecular and Cellular Pathology, University of Dundee, Dundee DD1 9SY, United Kingdom

Abstract:  The transcription coactivator p300 cannot acetylate native p53 tetramers, thus revealing intrinsic conformational constraints on p300-catalyzed acetylation. Consensus site DNA is an allosteric effector that promotes acetylation of p53, suggesting that p300 has an undefined conformationally flexible interface within the p53 tetramer. To identify such conformationally responsive p300-binding sites, p300 was subjected to peptide selection from a phage-peptide display library, a technique that can define novel protein-protein interfaces. The enriched p300-binding peptides contained a proline repeat (PXXP/PXPXP) motif, and five proline repeat motifs actually reside within the p53 transactivation domain, suggesting that this region of p53 may harbor the second p300 contact site. p300 binds in vitro to PXXP-containing peptides derived from the proline repeat domain, and PXXP-containing peptides inhibit sequence-specific DNA-dependent acetylation of p53, indicating that p300 docking to both the LXXLL and contiguous PXXP motif in p53 is required for p53 acetylation. Deletion of the proline repeat motif of p53 prevents DNA-dependent acetylation of p53 by occluding p300 from the p53-DNA complex. Sequence-specific DNA places an absolute requirement for the proline repeat domain to drive p53 acetylation in vivo. Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event. The PXXP repeat expands the basic interface of a p300-targeted transactivation domain, and proline-directed acetylation of p53 at promoters indicates that p300-mediated acetylation can be highly constrained by substrate conformation in vivo. 

Retracted: No

PubPeer comments:
 I was reading this interesting paper when I reached the part of flow cytometry... Besides than in Fig4 panel where there are some weird concentric artifacts, I have also spotted some suspicious duplications within theFC data Fig 5 in the upper panel. ![file] ,
(−)-Epicatechin prevents TNFα-induced activation of signaling cascades involved in inflammation and insulin sensitivity in 3T3-L1 adipocytes
Authors: Patricia I Oteiza
Fawaz G Haj
Ahmed Bettaieb
Marcela A Vazquez-Prieto
César G Fraga
Journal: Archives of Biochemistry and Biophysics (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Obesity; Chronic diseases; Inflammation; Adipose tissue; (-)-Epicatechin
Affiliations: Department of Pathology, School of Medicine, National University of Cuyo, Argentina.

Abstract:  Obesity is major public health concern worldwide and obese individuals exhibit a higher risk of chronic diseases such as type 2 diabetes. Inflammation plays a significant role in metabolic regulation and mounting evidence highlight the contribution of adipose tissue to systemic inflammatory state. Food extracts with a high content of (-)-epicatechin have been found to exert systemic anti-inflammatory actions, however the anti-inflammatory actions of (-)-epicatechin on adipose tissue remain to be determined. The aim of this study was to investigate the capacity of (-)-epicatechin to prevent tumor necrosis alpha (TNFα)-induced activation of cell signals involved in inflammation and insulin resistance (NF-κB, mitogen-activated protein kinases (MAPKs), AP-1, and peroxisome proliferator activated receptor γ (PPARγ)) in differentiated white adipocytes (3T3-L1). TNFα triggered the activation of transcription factors NF-κB and AP-1, and MAPKs ERK1/2, JNK, and p38. (-)-Epicatechin caused a dose (0.5-10 μM)-dependent decrease in TNFα-mediated JNK, ERK1/2, and p-38 phosphorylation, and nuclear AP-1-DNA binding. (-)-Epicatechin also inhibited TNFα-triggered activation of the NF-κB signaling cascade, preventing TNFα-mediated p65 nuclear transport and nuclear NF-κB-DNA binding. (-)-Epicatechin also attenuated the TNFα-mediated downregulation of PPARγ expression and decreased nuclear DNA binding. Accordingly, (-)-epicatechin inhibited TNFα-mediated altered transcription of genes (MCP-1, interleukin-6, TNFα, resistin, and protein-tyrosine phosphatase 1B) involved in inflammation and insulin signaling. In conclusion, (-)-epicatechin can attenuate TNFα-mediated triggering of signaling cascades involved in inflammation and insulin resistance. These findings could be of relevance in the dietary management of obesity and metabolic syndrome. 

Retracted: No

PubPeer comments:
 Concern about Figure 2. * Red boxes: The second lane in the p65 blot and the first lane in the hRNP blot look more similar than expected * Blue boxes: The first and fifth lanes in the p65 blot look more similar than expected ![file] Would the authors still have the original, uncropped blots to show here, please? ,
Phosphorylation of Tyr1214 within VEGFR-2 triggers the recruitment of Nck and activation of Fyn leading to SAPK2/p38 activation and endothelial cell migration in response to VEGF
Authors: François Houle
Laurent Lamalice
Jacques Huot
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: VEGFR-2; VEGF; phosphorylation; Tyr1214; Cdc42-SAPK2/p38-MAPKAP K2 pathway
Affiliations: Centre de Recherche en Cancérologie de l'Université Laval, 9 rue McMahon, Québec G1R 2J6, Canada.

Abstract:  VEGFR-2 is the major receptor that regulates the different functions of VEGF in adults. We have previously reported that following VEGF treatment of endothelial cells, VEGFR-2 is phosphorylated on Tyr1214 upstream of the Cdc42-SAPK2/p38-MAPKAP K2 pathway. However, little is known of the earliest molecular events that compose the SAPK2/p38 pathway following VEGFR-2 activation. In this study, we address this question using HA-tagged constructs of either wild-type VEGFR-2 or Y1214F VEGFR-2 mutant in immunoprecipitation assays. We show that the Src family kinase member Fyn, but not c-Src itself, is recruited to VEGFR-2 and is activated in a p-Tyr1214-dependent manner. We also report that the SH2 domain-containing adapter molecule Nck, but not Grb2, is recruited to VEGFR-2 in a p-Tyr1214-dependent manner and that it associates with Fyn. Moreover, PAK-2 is phosphorylated in a Fyn-dependent manner. Using chemical and genetic inhibitors, we show that Fyn activity is required for SAPK2/p38 but not for FAK activation in response to VEGF. In contrast, c-Src permits activation of FAK, but not that of SAPK2/p38. In addition, Fyn is required for stress fiber formation and endothelial cell migration. We propose a model in which Fyn forms a molecular complex with Nck and PAK-2 and suggest that this complex assembles in a p-Tyr1214-dependent manner within VEGFR-2 following VEGF treatment. In turn, this triggers the activation of the SAPK2/p38 MAP kinase module, and promotes stress fiber formation and endothelial cell migration. 

Retracted: No

PubPeer comments:
 ![file] ,
Synthesis of oxovanadium(IV) Schiff base complexes derived from C-substituted diamines and pyridoxal-5-phosphate as antitumor agents
Authors: Shubhra Chaturvedi
Bilikere Srinivasarao Dwarakanath
Puja Panwar Hazari
Sudhir Chandna
Anil Kumar Mishra
Anjani Kumar Tiwari
Anand Kumar Pandey
Journal: Chemical Biology & Drug Design (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Oxovanadium (IV) complexes; DNA cleavage; nuclease activity; tumor regression; salen derivatives
Affiliations: Division of Cyclotron and Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, Brig SK Mazumdar Road, New Delhi 110054, India. 

Abstract:  Oxovanadium (IV) complexes of N,N'-bispyridoxyl-5, 5'-bis (phosphate) ethylenediimine (L1) and N,N'-bis(pyridoxyl)-5,5'-bis(phosphate)-1''-(p-nitrobenzyl)ethylenediimine (L2) were synthesized by condensation of optically active C-substituted diamines and pyridoxal-5-phosphate. Oxovanadium (IV) complexes derived from L1 and L2 were evaluated as DNA cleavage agent (cleavage of supercoiled plasmid pBR322 DNA). Interestingly, both the oxovanadium (IV) complexes exhibited DNA nuclease activity, and the extent of oxidation of DNA by these vanadyl complexes was superior to VOSO(4) . The significant reduction in primary tumor and increased delay in tumor growth of 15 days was seen in the tumor regression analysis with oxovanadium (IV) complex of L1. With the preliminary studies performed with the pyridoxal-5-phosphate -based salen derivatives including the cytotoxicity and tumor regression, it is evident that the salen bifunctional chelating agent has obtained therapeutic potential if conjugated to a gene-specific targeting molecule for the oxidation of guanine residue. 

Retracted: No

PubPeer comments:
 ![file] ,
The dietary polysaccharide maltodextrin promotes Salmonella survival and mucosal colonization in mice
Authors: Carol A de la Motte
Kourtney P Nickerson
Laura J Dixon
Erin E Johnson
Ilyssa O Gordon
Christine McDonald
Amrita Kabi
Sean P Kessler
Craig R Homer
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: American diet; processed foods; dietary fiber; Salmonella; chronic inflammatory diseases
Affiliations: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America; Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio, United States of America., Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America., Department of Anatomic Pathology, Robert J. Tomsich Pathology & Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, United States of America., Department of Biology, John Carroll University, University Heights, Ohio, United States of America.

Abstract:  In the latter half of the 20th century, societal and technological changes led to a shift in the composition of the American diet to include a greater proportion of processed, pre-packaged foods high in fat and carbohydrates, and low in dietary fiber (a "Western diet"). Over the same time period, there have been parallel increases in Salmonella gastroenteritis cases and a broad range of chronic inflammatory diseases associated with intestinal dysbiosis. Several polysaccharide food additives are linked to bacterially-driven intestinal inflammation and may contribute to the pathogenic effects of a Western diet. Therefore, we examined the effect of a ubiquitous polysaccharide food additive, maltodextrin (MDX), on clearance of the enteric pathogen Salmonella using both in vitro and in vivo infection models. When examined in vitro, murine bone marrow-derived macrophages exposed to MDX had altered vesicular trafficking, suppressed NAPDH oxidase expression, and reduced recruitment of NADPH oxidase to Salmonella-containing vesicles, which resulted in persistence of Salmonella in enlarged Rab7+ late endosomal vesicles. In vivo, mice consuming MDX-supplemented water had a breakdown of the anti-microbial mucous layer separating gut bacteria from the intestinal epithelium surface. Additionally, oral infection of these mice with Salmonella resulted in increased cecal bacterial loads and enrichment of lamina propria cells harboring large Rab7+ vesicles. These findings indicate that consumption of processed foods containing the polysaccharide MDX contributes to suppression of intestinal anti-microbial defense mechanisms and may be an environmental priming factor for the development of chronic inflammatory disease. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: The right-most sICAM band looks remarkably similar to the right-most MCP-1 band. Reported to the journal in October 2015, but no action taken as of today. ![file] ,