PReD-Bench/PRed-Bench huggingface dataset:
MicroRNA-613 impedes the proliferation and invasion of glioma cells by targeting cyclin-dependent kinase 14
Authors: Lei Zhou
Maode Wang
Qi Li
Lei Qi
Chuankun Li
Jia Wang
Ning Wang
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: CDK14; Glioma; Wnt; miR-613.
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China. Electronic address: ., Department of Ultrasonography, Xi'an No. 4 Hospital, Xi'an, Shaanxi 710004, China., Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.

Abstract:  Increasing evidence has suggested that microRNAs (miRNAs) are critical regulators of tumorigenesis. MicroRNA-613 (miR-613) has recently been reported as a novel tumor-related miRNA that plays an important role in multiple cancers. However, the expression and functional significance of miR-613 in glioma remains unclear. In this study, we aimed to investigate the biological function of miR-613 in glioma. We found that miR-613 expression was frequently downregulated in glioma tissues and cell lines compared with normal controls. Overexpression of miR-613 impeded proliferation and colony formation and induced cell cycle arrest in G0/G1 phase, and also inhibited the invasive ability of glioma cells. By contrast, miR-613 inhibition had the opposite effects. Bioinformatic analysis and dual-luciferase reporter assays showed that miR-613 directly targets the 3'-untranslated region of cyclin-dependent kinase 14 (CDK14). Real-time quantitative PCR and Western blot analysis showed that CDK14 expression is negatively regulated by miR-613. In addition, miR-613 expression was inversely correlated with CDK14 expression in clinical glioma tissues. Moreover, overexpression of miR-613 decreased the protein expression of β-catenin and inhibited the activation of Wnt signaling. Importantly, the antitumor effects of miR-613 were significantly reversed by CDK14 overexpression. Overall, our results show that miR-613 inhibits glioma cell proliferation and invasion by downregulating CDK14, suggesting that miR-613 and CDK14 may serve as potential therapeutic targets for the treatment of glioma. 

Retracted: No

PubPeer comments:
 Fig 2D. ![file] I have not tried to be exhaustive. More easter eggs remain. Fig 6D. ![file] , 
 #1 For Fig 2D, add a couple of more. Still, maybe more out there. ![file] ,
Constitutive expression of ULBP-4 on monocytes regulates NK cell NKG2D expression
Authors: Mary A Markiewicz
Neekun Sharma
Journal: Blood advances (2019)
Discipline: CLINICAL MEDICINE
Keywords: NKG2D ligand; ULBP-4; monocytes; NK cells; regulation
Affiliations: Department of Microbiology, Molecular Genetics & Immunology, University of Kansas Medical Center, Kansas City, KS.

Abstract:  The NKG2D ligand ULBP-4 is expressed on healthy monocytes.Monocyte ULBP-4 expression regulates NKG2D expression by NK cells. 

Retracted: No

PubPeer comments:
 Readers should become aware of a recent preprint entitled  The NKG2D ligand ULBP4 is not expressed by human monocytes deposited at bioRxiv . From the abstract:  Here, we scrutinized ULBP4 expression by human peripheral blood mononuclear cells and monocytes by analyzing ULBP4 transcripts and ULBP4 surface expression. In contrast to MICA, there was no ULBP4 expression detectable, neither by freshly isolated monocytes nor by PAMP-activated monocytes. **However, a commercial antibody erroneously indicated surface ULBP4 on monocytes due to a non-ULBP4-specific binding activity, emphasizing the critical importance of validated reagents for life sciences.** Collectively, our data show that ULBP4 is not expressed by monocytes, and likely also not by other peripheral blood immune cells, and therefore exhibits an expression pattern rather distinct from other human NKG2DL ,
Opaque7 encodes an acyl-activating enzyme-like protein that affects storage protein synthesis in maize endosperm
Authors: Rentao Song
Gang Wang
Jinsheng Lai
Xiaoliang Sun
Chong Chang
Zhengkai Xu
Fei Wang
Lihuang Zhu
Guifeng Wang
Xin Sun
Yuanping Tang
Qiang Gao
Journal: Genetics (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: maize; seed mutants; starchy endosperm; lysine content; zeins accumulation
Affiliations: Shanghai Key Laboratory of Bioenergy Crops, School of Life Sciences, Shanghai University, Shanghai 200444, China, State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100101, China, The State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China

Abstract:  In maize, a series of seed mutants with starchy endosperm could increase the lysine content by decreased amount of zeins, the main storage proteins in endosperm. Cloning and characterization of these mutants could reveal regulatory mechanisms for zeins accumulation in maize endosperm. Opaque7 (o7) is a classic maize starchy endosperm mutant with large effects on zeins accumulation and high lysine content. In this study, the O7 gene was cloned by map-based cloning and confirmed by transgenic functional complementation and RNAi. The o7-ref allele has a 12-bp in-frame deletion. The four-amino-acid deletion caused low accumulation of o7 protein in vivo. The O7 gene encodes an acyl-activating enzyme with high similarity to AAE3. The opaque phenotype of the o7 mutant was produced by the reduction of protein body size and number caused by a decrease in the α-zeins concentrations. Analysis of amino acids and metabolites suggested that the O7 gene might affect amino acid biosynthesis by affecting α-ketoglutaric acid and oxaloacetic acid. Transgenic rice seeds containing RNAi constructs targeting the rice ortholog of maize O7 also produced lower amounts of seed proteins and displayed an opaque endosperm phenotype, indicating a conserved biological function of O7 in cereal crops. The cloning of O7 revealed a novel regulatory mechanism for storage protein synthesis and highlighted an effective target for the genetic manipulation of storage protein contents in cereal seeds. 

Retracted: No

PubPeer comments:
 **Fig. 11 B, C, D** ![file] , 
 # Fig. 11 D and Fig. 12 A ![file] , 
 # Fig. 6 B ![file] **Pseudo Colored Comparison** ![file] , 
 # Fig. 7 C ![file] , 
 # Fig. 12B # ![file] , 
 # Fig. 6 B # ![file] **Pseudo Colored Comparison** ![file] ,
Real-time PCR assay is superior to other methods for the detection of mycoplasma contamination in the cell lines of the National Cell Bank of Iran
Authors: Arash Memarnejadian
Shahram Azari
Vahid Molla Kazemiha
Mohammad Ali Shokrgozar
Shahin Bonakdar
Shirin Shahbazi
Amir Amanzadeh
Reza Mahdian
Journal: Cytotechnology (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell culture; DAPI staining; Mycoplasma contamination; PCR; Real-time PCR.
Affiliations: National Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran., Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, Iran., Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran., National Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran. ., Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran. .

Abstract:  Mycoplasmas are the most important contaminants of cell cultures throughout the world. They are considered as a major problem in biological studies and biopharmaceutical economic issues. In this study, our aim was to find the best standard technique as a rapid method with high sensitivity, specificity and accuracy for the detection of mycoplasma contamination in the cell lines of the National Cell Bank of Iran. Thirty cell lines suspected to mycoplasma contamination were evaluated by five different techniques including microbial culture, indirect DNA DAPI staining, enzymatic mycoalert(®) assay, conventional PCR and real-time PCR. Five mycoplasma-contaminated cell lines were assigned as positive controls and five mycoplasma-free cell lines as negative controls. The enzymatic method was performed using the mycoalert(®) mycoplasma detection kit. Real-time PCR technique was conducted by PromoKine diagnostic kits. In the conventional PCR method, mycoplasma genus-specific primers were designed to analyze the sequences based on a fixed and common region on 16S ribosomal RNA with PCR product size of 425 bp. Mycoplasma contamination was observed in 60, 56.66, 53.33, 46.66 and 33.33 % of 30 different cell cultures by real-time PCR, PCR, enzymatic mycoalert(®), indirect DNA DAPI staining and microbial culture methods, respectively. The analysis of the results of the different methods showed that the real-time PCR assay was superior the other methods with the sensitivity, specificity, accuracy, predictive value of positive and negative results of 100 %. These values were 94.44, 100, 96.77, 100 and 92.85 % for the conventional PCR method, respectively. Therefore, this study showed that real-time PCR and PCR assays based on the common sequences in the 16S ribosomal RNA are reliable methods with high sensitivity, specificity and accuracy for detection of mycoplasma contamination in cell cultures and other biological products. 

Retracted: No

PubPeer comments:
 Figure 1a (right panel) appears to have two images which overlap, after dimensions and colors are changed, and some features altered in upper left corner of these samples (green and yellow). Difficult to see how all this could occur merely in error during figure assembly. *** ![file] ,
Endothelial toll‐like receptor 4 maintains lung integrity via epigenetic suppression of p16 INK4a
Authors: Patty J Lee
Alfred Li
So-Jin Kim
Tien Peng
Yi Zhang
Taylor Ardito
Peiying Shan
Cheol Hwangbo
Maor Sauler
Jin-Na Min
Xuchen Zhang
Journal: Aging Cell (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HDAC2; aging; cellular senescence; emphysema; p16INK4a
Affiliations: Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut., Division of Applied Life Science (BK21 Plus), PMBBRC, Division of Life Science, College of National Sciences, Gyeongsang National University, Jinju, Korea., Department of Pathology, Yale University School of Medicine, New Haven, Connecticut., Bone Imaging Research Core, University of California, San Francisco (UCSF), San Francisco, California., Department of Medicine, Cardiovascular Research Institute, UCSF, San Francisco, California.

Abstract:  We previously reported that the canonical innate immune receptor toll-like receptor 4 (TLR4) is critical in maintaining lung integrity. However, the molecular mechanisms via which TLR4 mediates its effect remained unclear. In the present study, we identified distinct contributions of lung endothelial cells (Ec) and epithelial cells TLR4 to pulmonary homeostasis using genetic-specific, lung- and cell-targeted in vivo methods. Emphysema was significantly prevented via the reconstituting of human TLR4 expression in the lung Ec of TLR4-/- mice. Lung Ec-silencing of TLR4 in wild-type mice induced emphysema, highlighting the specific and distinct role of Ec-expressed TLR4 in maintaining lung integrity. We also identified a previously unrecognized role of TLR4 in preventing expression of p16INK4a , a senescence-associated gene. Lung Ec-p16INK4a -silencing prevented TLR4-/- induced emphysema, revealing a new functional role for p16INK4a in lungs. TLR4 suppressed endogenous p16INK4a expression via HDAC2-mediated deacetylation of histone H4. These findings suggest a novel role for TLR4 in maintaining of lung homeostasis via epigenetic regulation of senescence-related gene expression. 

Retracted: No

PubPeer comments:
 Figure 3 (f) actin and Figure 5 (b) actin appear to be the same image. (they are in different condition, therefore the actins could not be the same) In the image below I have adjusted these settings to match, and added some red boxes and lines to highlight a few of the distinctive features which are in both sections. ![file] ![file] ![file] Also, Figure 5 (k) p-HDAC and HDAC2 s right sections appear to be the same image, with different brightness contrast. In the image below I have adjusted these settings to match, and added some red circles and lines to highlight a few of the distinctive features which are in both sections. ![file] ,
Interposed abdominal compression-cardiopulmonary resuscitation after cardiac surgery
Authors: Jun Wang
Tian-fa Li
Ji-ke Li
Journal: Interactive cardiovascular and thoracic surgery (2014)
Discipline: CLINICAL MEDICINE
Keywords: Cardiac arrest; Cardiac surgery; Conventional cardiopulmonary resuscitation; Interposed abdominal compression-cardiopulmonary resuscitation.

Abstract:  Objectives: The management of cardiac arrest after cardiac surgery differs from the management of cardiac arrest under other circumstances. In other studies, interposed abdominal compression-cardiopulmonary resuscitation (IAC-CPR) resulted in a better outcome compared with conventional CPR. The aim of the present study was to determine the feasibility, safety and efficacy of IAC-CPR compared with conventional CPR in patients with cardiac arrest after cardiac surgery. Methods: Data on all cardiac surgical patients who suffered a sudden cardiac arrest during the first 24 h after surgery were collected prospectively. Cardiac arrest was defined as the cessation of cardiac mechanical activity with the absence of a palpable central pulse, apnoea and unresponsiveness, including ventricular fibrillation, asystole and pulseless electrical activity. Forty patients were randomized to either conventional CPR (n = 21) or IAC-CPR (n = 19). IAC-CPR was initially performed by compressing the abdomen midway between the xiphoid and the umbilicus during the relaxation phase of chest compression. If spontaneous circulation was not restored after 10-15 min, the surgical team would immediately proceed to resternotomy. The endpoints of the study were safety, return of spontaneous circulation (ROSC) &gt;5 min, survival to hospital discharge and survival for 6 months. Results: With IAC-CPR, there were more patients in terms of ROSC, survival to hospital discharge, survival for 6 months and fewer CPR-related injuries compared with patients who underwent conventional CPR. Conclusions: IAC-CPR is feasible and safe and may be advantageous in cases of cardiac arrest after cardiac surgery. 

Retracted: Yes

PubPeer comments:
 Retracted on 25 August 2019. Copy pasted from https: academic.oup.com icvts advance-article doi 10.1093 icvts ivz200 5554425  In response to concerns expressed by a reader regarding the validity of the data reported in this article, the Editorial Office of Interactive CardioVascular and Thoracic Surgery tried to contact the authors for clarification and rectification. Several emails were sent to the corresponding author, Dr Tian-fa Li, with co-authors copied on a number of the reminders. Attempts to reach the authors by telephone and fax were also unsuccessful. After an assessment by 2 of our statistical reviewers, it was concluded that all P-values and percentages seem to be incorrect and that the contents of the article are misleading. In light of these findings and the authors failure to respond, the Editor-in-Chief has decided to retract this article. ,
Coldzyme® Mouth Spray reduces duration of upper respiratory tract infection symptoms in endurance athletes under free living conditions
Authors: Gabriella M Swart
Arwel W Jones
Eleanor Perkins
Hayley Robinson
Alex R Jenkins
Glen Davison
Kimberly Dargan
Journal: European Journal of Sport Science (2020)
Discipline: CLINICAL MEDICINE
Keywords: Common cold; countermeasure; exercise; illness; immunology
Affiliations: Endurance Research Group, School of Sport & Exercise Sciences, University of Kent, UK, Lincoln Institute for Health, University of Lincoln, Lincoln, UK.

Abstract:  Upper respiratory tract infection (URTI) can compromise athlete preparation and performance, so countermeasures are desirable. The aim of this study was to assess the effects of ColdZyme® Mouth Spray (ColdZyme) on self-reported upper respiratory tract infection in competitive endurance athletes under free-living conditions. One hundred and twenty-three endurance-trained, competitive athletes (recruited across 4 sites in England, UK) were randomised to control (no treatment, n = 61) or ColdZyme (n = 62) for a 3-month study period (between December 2017 and March 2018; or December 2018 and April 2019). They recorded daily training and illness symptoms (Jackson common cold questionnaire) during the study period. A total of 130 illness episodes were reported during the study with no difference in incidence between groups (episodes per person: 1.1 ± 0.9 Control, 1.0 ± 0.8 ColdZyme, P = 0.290). Episode duration was significantly shorter in ColdZyme compared to Control: Control 10.4 ± 8.5 days vs. ColdZyme 7.7 ± 4.0 days, P = 0.016). Further analysis to compare episodes with poor vs. good compliance with ColdZyme instructions for use (IFU) within the ColdZyme group showed a greater reduction in duration of URTI when compliance was good (9.3 ± 4.5 days in ColdZyme poor IFU compliance vs. 6.9 ± 3.5 days in ColdZyme good IFU compliance, P = 0.040). ColdZyme may be an effective countermeasure to reduce URTI duration, which was significantly lower (by 26-34%) in the ColdZyme treatment group (with no influence on incidence). This may have implications for athlete performance. 

Retracted: No

PubPeer comments:
 Can the authors supply the data per person and per episode and clarify how they performed their statistics? Can they explain the following statistical differences (as the CIs (if they are CIs) are completely overlapping). - Days until recovery: Control 10.4u2009u00b1u20098.5 days vs ColdZyme 7.7u2009u00b1u20094.0 days, Pu2009=u20090.016 - Jackson Symptom Score (episode total): t74.9u2009u00b1u200972.0 vst**43.6u2009u00b1u200930.1: Jackson Symptom Score (daily episode average)t6.9u2009u00b1u20092.8t**5.5u2009u00b1u20092.4 - Days missedt3.5u2009u00b1u20095.0t*1.6u2009u00b1u20092.5: same remark ,
The principle of inverse effectiveness in multisensory integration: some statistical considerations
Authors: Nicholas P Holmes
Journal: Brain Topography (2009)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Principle of Inverse Effectiveness; Multisensory Integration; Regression towards the mean; Stimulus intensity; Neurophysiological constraints
Affiliations: Department of Psychology & Interdisciplinary Center for Neural Computation, Hebrew University of Jerusalem, Jerusalem, 91905, Israel. 

Abstract:  The principle of inverse effectiveness (PoIE) in multisensory integration states that, as the responsiveness to individual sensory stimuli decreases, the strength of multisensory integration increases. I discuss three potential problems in the analysis of multisensory data with regard to the PoIE. First, due to 'regression towards the mean,' the PoIE may often be observed in datasets that are analysed post-hoc (i.e., when sorting the data by the unisensory responses). The solution is to design discrete levels of stimulus intensity a priori. Second, due to neurophysiological or methodological constraints on responsiveness, the PoIE may be, in part, a consequence of 'floor' and 'ceiling' effects. The solution is to avoid analysing or interpreting data that are too close to the limits of responsiveness, enabling both enhancement and suppression to be reliably observed. Third, the choice of units of measurement may affect whether the PoIE is observed in a given dataset. Both relative (%) and absolute (raw) measurements have advantages, but the interpretation of both is affected by systematic changes in response variability with changes in response mean, an issue that may be addressed by using measures of discriminability or effect-size such as Cohen's d. Most importantly, randomising or permuting a dataset to construct a null distribution of a test parameter may best indicate whether any observed inverse effectiveness specifically characterises multisensory integration. When these considerations are taken into account, the PoIE may disappear or even reverse in a given dataset. I conclude that caution should be exercised when interpreting data that appear to follow the PoIE. 

Retracted: No

PubPeer comments:
 Fig 4a.  The apoptosis of bone cells of rats in each group detected via TUNEL staining . ![] Unexpected similarities. Now let s zoom in on just two panels: ![file] ------------------------------------- Fig 3b. ![] Fig 3c. ![file] , 
  **Acknowledgments** We would like to acknowledge the reviewers for their helpful comments on this pap. ,
Dissecting the Protein Dynamics Coupled Ligand Binding with Kinetic Models and Single-Molecule FRET
Authors: Wenjie Huang
Shijuan Yan
Wenkang Wei
Shaowen Wu
Wenyang Zhang
Qian Kong
Zhongjian Chen
Wenyan Li
Journal: Biochemistry (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Protein-ligand interactions; conformational dynamics; ligand binding; dissociation; single-molecule FRET
Affiliations: Guangdong Key Laboratory for Crop Germplasm Resources Preservation and Utilization, Agro-biological Gene Research Center, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, Guangdong, China.

Abstract:  Protein-ligand interactions are crucial to many biological processes. Ligand binding and dissociation are the basic steps that allow proteins to function. Protein conformational dynamics have been shown to play important roles in ligand binding and dissociation. However, it is challenging to determine the ligand binding kinetics of dynamic proteins. Here, we undertook comprehensive single-molecule FRET (smFRET) measurements and kinetic model analysis to characterize the conformational dynamics coupled ligand binding of glutamine-binding protein (GlnBP). We showed that hinge and T118A mutations of GlnBP affect its conformational dynamics as well as the ligand binding affinity. Based on smFRET measurements, the kinetic model of ligand-GlnBP interactions was constructed. Using experimentally measured parameters, we solved the rate equations of the model and obtained the undetectable parameters of the model which allowed us to understand the ligand binding kinetics fully. Our results demonstrate that modulation of the conformational dynamics of GlnBP affects the ligand binding and dissociation rates. This study provides insights into the binding kinetics of ligands, which are related to the protein function itself. 

Retracted: No

PubPeer comments:
 The authors cite wrong references to support their claims, thus misleading the reader and attempting to distort published evidence that is in total disagreement with their findings. For example reference 33 in the following sentence, reported the exact opposite of what the authors claim:  NMR residual dipolar couplings, smFRET, and phosphorescence spectroscopy experiments suggested that multiple states of GlnBP coexist. (24,32,33) ,
Effects of growth hormone on bone modeling and remodeling in hypophysectomized young female rats: a bone histomorphometric study
Authors: Lysette Iglesias
Mariano Castro-Magana
John F Aloia
James K Yeh
Journal: Journal of Bone and Mineral Metabolism (2011)
Discipline: CLINICAL MEDICINE
Keywords: Growth hormone; bone modeling; bone remodeling; hypophysectomized rats; bone density
Affiliations: Department of Pediatric Endocrinology, Winthrop University Hospital, 120 Professional Building Suite 210, Mineola, NY 11501, USA. 

Abstract:  Growth hormone (GH) deficiency causes decreased bone mineral density and osteoporosis, predisposing to fractures. We investigated the mechanism of action of GH on bone modeling and remodeling in hypophysectomized (HX) female rats. Thirty female Sprague-Dawley rats at age 2 months were divided into three groups with 10 rats each: control (CON) group, HX group, and HX + GH (3 mg/kg daily s.c.) group, for a 4-week study. Hypophysectomy resulted in cessation of bone growth and decrease in cancellous bone mass. Periosteal bone formation decreased and bone turnover rate of endocortical and trabecular surfaces increased as compared to the CON group. GH administration for 4 weeks restored weight gain and bone growth and mitigated decrease in bone density after hypophysectomy. However, trabecular bone mass in the proximal tibial metaphysis remained lower in group HX + GH than in group CON. Dynamic histomorphometric analysis showed that bone modeling of periosteal bone formation and growth plate elongation was significantly higher in group HX + GH than in group HX. New bone formed beneath the growth plate was predominately woven bone in group CON and group HX + GH. Bone remodeling and modeling-remodeling mixed modes in the endocortical and PTM sites were enhanced by GH administration; both bone formation and resorption activities were significantly higher than in group HX. In conclusion, GH administration to HX rats reactivated modeling activities in modeling predominant sites and increased new bone formation. GH administration also increases remodeling activities in remodeling predominant sites, giving limited net gain in the bone mass. 

Retracted: No

PubPeer comments:
 Figure 1 is not consistent with Definition 6 (the key notion of this paper), which itself is confusing. In Definition 6, the terms $$gamma^+ = max( gamma^k(p_k))$$ and $$gamma^- = min( gamma^k(p_k))$$ are confusing along with the terms $p^+$ and $p^-$ being the corresponding probabilities. If it means $$gamma^+ = max (gamma^k)$$ $$gamma^- = min (gamma^k)$$ then the corresponding $p^+$ may not be the largest value as illustrated in Figure 1. If it means $$gamma^+ = max (gamma^ktimes p^k)$$ $$gamma^- = min (gamma^ktimes p^k)$$ Then the corresponding $gamma^+$ may not be the largest value as illustrated in Figure 1. In either case, the upper area $a(h)^+$ and the lower area $a(h)^-$ defined in Definition 6 are not clear in this context and not consistent with the illustration in Figure 1. ![file] , 
 #1 ![file] ,
Gastrointestinal Pathologic Abnormalities in Pediatric- and Adult-Onset Common Variable Immunodeficiency
Authors: Alberto Ravelli
Alberto Lanzini
Maurizio Fuoti
Alessandro Plebani
Gabrio Bassotti
Vassilios Lougaris
Francesco Lanzarotto
Marianna Salemme
Vincenzo Villanacci
Annarosa Soresina
Journal: Digestive diseases and sciences (2015)
Discipline: CLINICAL MEDICINE
Keywords: Common variable immunodeficiency; gastrointestinal manifestations; histopathological findings; pediatric; adult
Affiliations: Pediatrics Clinic, Department of Clinical and Experimental Sciences, Spedali Civili, University of Brescia, Brescia, Italy.

Abstract:  Background: Common variable immunodeficiency is the most common form of primary symptomatic immunodeficiency. Gastrointestinal manifestations, such as gastritis, diarrhea, gastrointestinal infections, and malabsorption, may complicate the clinical history in almost 50 % of patients. Aim: To evaluate gastrointestinal histopathological findings in pediatric- and in adult-onset common variable immunodeficiency patients. Methods: Twenty-two patients with common variable immunodeficiency (13 children, nine adults) were retrospectively studied from a clinical and histopathological point of view. Results: Increased T lymphocyte infiltrate and the absence of plasma cells in duodenal lamina propria and submucosa were the most frequent findings, independently from onset age, whereas follicular lymphoid hyperplasia and polymorphonuclear infiltrate, as well as parasitic and viral infections, were only present in the adult group. Common variable immunodeficiency patients with minor gastrointestinal symptoms also presented pathological findings, mainly the absence of plasma cells, T cell infiltrate, and infections, independently of age. Conclusions: Gastrointestinal pathological abnormalities are common in both pediatric- and adult-onset common variable immunodeficiency patients. Histological alterations may vary depending upon the age of onset, possibly due to duration of disease. Minor gastrointestinal symptoms are also associated with pathological findings; therefore, these should be searched in all symptomatic patients. 

Retracted: No

PubPeer comments:
 Now available in print with linked editorial: T Jefferson, E A Spencer, J Brassey, C Heneghan, Viral cultures for COVID-19 infectious potential assessment u2013 a systematic review, Clinical Infectious Diseases, Dec 3, 2020. https: doi.org 10.1093 cid ciaa1764T Jefferson, E A Spencer, J Brassey, C Heneghan, Viral cultures for COVID-19 infectious potential assessment u2013 a systematic review, Clinical Infectious Diseases, Dec 3, 2020. https: doi.org 10.1093 cid ciaa1764 Peter Doshi, John H Powers, III, Determining the infectious potential of individuals with positive RT-PCR SARS-CoV-2 tests, Clinical Infectious Diseases, Dec 4, 2020, https: doi.org 10.1093 cid ciaa1819 ,
Dentate gyrus neurons that are born at the peak of development, but not before or after, die in adulthood
Authors: Jason S Snyder
Tina Ciric
Shaina P Cahill
Journal: Brain and Behavior (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: cell death; development; neurogenesis; ontogeny; plasticity
Affiliations: Department of Psychology, Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, Canada.

Abstract:  Introduction: In the dentate gyrus of the rodent hippocampus, neurogenesis begins prenatally and continues to the end of life. Adult-born neurons often die in the first few weeks after mitosis, but those that survive to 1 month persist indefinitely. In contrast, neurons born at the peak of development are initially stable but can die later in adulthood. Physiological and pathological changes in the hippocampus may therefore result from both the addition of new neurons and the loss of older neurons. The extent of neuronal loss remains unclear since no studies have examined whether neurons born at other stages of development also undergo delayed cell death. Methods: We used BrdU to label dentate granule cells that were born in male rats on embryonic day 19 (E19; before the developmental peak), postnatal day 6 (P6; peak), and P21 (after the peak). We quantified BrdU+ neurons in separate groups of rats at 2 and 6 months post-BrdU injection to estimate cell death in young adulthood. Results: Consistent with previous work, there was a 15% loss of P6-born neurons between 2 and 6 months of age. In contrast, E19- or P21-born neurons were stable throughout young adulthood. Discussion: Delayed death of P6-born neurons suggests these cells may play a unique role in hippocampal plasticity adulthood, for example, by contributing to the turnover of hippocampal memory. Their loss may also play a role in disorders that are characterized by hippocampal atrophy. 

Retracted: No

PubPeer comments:
 When this was a preprint, there was some discussion about whether the death of adult-born neurones was physiological or induced by BdrU. https: pubpeer.com publications 66B7440A4ED82B00343B7ECD629CE4 ,
Diminution of microRNA-98 alleviates renal fibrosis in diabetic nephropathy by elevating Nedd4L and inactivating TGF-β/Smad2/3 pathway
Authors: Ming Yang
Yi Zeng
Zhenkun He
Yihua Bai
Yunjuan Liao
Zhijian Feng
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Diabetic nephropathy; apoptosis; microRNA-98; neural precursor cell expressed developmentally downregulated gene 4-like; renal fibrosis
Affiliations: Nephrology Department, The Second Affiliated Hospital of Kunming Medical University , Kunming, Yunnan, China.

Abstract:  MicroRNAs (miRNAs) have already been documented to function in diabetic nephropathy (DN), yet little research has focused on the role of miR-98 in this disease. Here, we discuss the mechanism of miR-98 on the renal fibrosis in DN. Recombinant adeno-associated virus carrying miR-98 inhibitor or Nedd4L overexpression plasmid was injected into DN modeled rats to explore their roles in DN. Renal tubular epithelial cell injury models (NRK-52E cells) were induced by high glucose (HG). HG-treated NRK-52E cells were transfected with miR-98 inhibitor or Nedd4L overexpression plasmid for further verification. MiR-98 was upregulated, Nedd4L was downregulated and TGF-β/Smad2/3 signaling was activated in kidney tissues of DN rats and HG-treated NRK-52E cells. miR-98 targeted Nedd4L mRNA 3'UTR. MiR-98 depletion and Nedd4L overexpression inactivated TGF-β/Smad2/3 signaling pathway, alleviated pathological damage and fibrosis, ameliorated inflammation, and depressed cell apoptosis of kidney tissues of DN rats. MiR-98 depletion and Nedd4L overexpression inactivated TGF-β/Smad2/3 signaling pathway, strengthened viability, and limited apoptosis of HG-treated renal tubular epithelial cells. Nedd4L overexpression reversed the effect of up-regulating miR-98 on DN rats and HG-treated renal tubular epithelial cells. Altogether, we find that miR-98 is upregulated in kidney tissues of DN rats, and miR-98 diminution and Nedd4L elevation attenuate renal fibrosis through inactivation of the TGF-β/Smad2/3 pathway, which provides a novel therapy for DN. 

Retracted: No

PubPeer comments:
 Figs 4d,e; 7b,c,d. These are curiously stylised Western Blots, almost geometrical in their perfection. Is it possible for the authors to upload scans of the original blots? ![file]  We would like to acknowledge the reviewers for their helpful comments on this pap. I have encountered this specific Acknowledgement at the end of about a dozen other problematical papers, hence my concern here. ,
Effect of 3:7 ratio of Astragalus total saponins and Curcumin on the diabetic nephropathy rats model
Authors: Tianyuan Liu
Baosong Liu
Jinxin Miao
Mingsan Miao
Mengfan Peng
Journal: Saudi Journal of Biological Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Astragalus total saponins; Curcumin; Diabetic nephropathy; Glycometableolism; Lipid metableolism
Affiliations: Department of Pharmacology, Henan University of Chinese Medicine, Zhengzhou 450046, China.

Abstract:  Objective: Study the effect of the 3:7 ratio of Astragalus total saponins and Curcumin on the model of diabetic nephropathy rats, and explore its mechanisms. Methods: Diabetic nephropathy rats model was established by high-fat and high-sugar feed feeding combined with streptozotocin (STZ) injection in sublingual vein. Measured fasting blood glucose of rats on the 10, 20 and 30th day, and measured urine protein content in urine of rats on 30th days. Two hours after the last administration, measured glycated serum protein (GSP), insulin antibody (IA), triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), malondialdehyde (MDA), insulin, superoxide dismutase (SOD), glutathione (GSH), urea nitrogen (BUN), creatinine (Cr) in the serum and calculated the renal index of rat. Take the viscera of pancreas and kidney, and HE staining, so as to observe pathological changes. Result: Astragalus total saponins and Curcumin 3:7 compatibility each dose group can significantly reduce the diabetic nephropathy rats blood glucose of 30th days, significantly reduce the level of GSP, IA, TG, TC, LDL (P &lt; 0.01), and reduce MDA levels with different degrees (P &lt; 0.01 or P &lt; 0.05), and significantly increase the level of insulin (P &lt; 0.01), increase the level of HDL, SOD and GSH with different degrees (P &lt; 0.01 or P &lt; 0.05 or P &gt; 0.05); Astragalus total saponins and Curcumin 3:7 compatibility each dose group also can decrease renal index, UN, and Cr levels with different degrees and improve the pathological changes of pancreatic tissue and kidney tissue in diabetic nephropathy rats with different degrees (P &lt; 0.01 or P &lt; 0.05 or P &gt; 0.05). Conclusion: The 3:7 ratio of Astragalus total saponins and Curcumin can achieve the treatment and protection effects on diabetic nephropathy rats by improve the glycometableolism, insulin resistance, lipid metableolism, oxidative stress levels, and pathological changes. 

Retracted: No

PubPeer comments:
 Figure 15 and 16 are labelled differently but show the same set of images. Would the authors please comment? ![file] , 
 Dear Mycosphaerella arachidis. Thank you for your seriousness and carefulness. The photo upload error was also found during the self-examination of the paper. We have contacted the magazine and will issue Corrigendum in the near future. ,
Greater fuel efficiency is potentially preferable to reducing NOx emissions for aviation’s climate impacts
Authors: Rubén Rodríguez De León
Agnieszka Skowron
David S Lee
Bethan Owen
Ling L Lim
Journal: Nature Communications (2021)
Discipline: Multidisciplinary
Keywords: Aviation emissions; nitrogen oxides; atmosphere composition; greenhouse gases; ozone
Affiliations: Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, UK. ., Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, UK.

Abstract:  Aviation emissions of nitrogen oxides (NOx) alter the composition of the atmosphere, perturbing the greenhouse gases ozone and methane, resulting in positive and negative radiative forcing effects, respectively. In 1981, the International Civil Aviation Organization adopted a first certification standard for the regulation of aircraft engine NOx emissions with subsequent increases in stringency in 1992, 1998, 2004 and 2010 to offset the growth of the environmental impact of air transport, the main motivation being to improve local air quality with the assumed co-benefit of reducing NOx emissions at altitude and therefore their climate impacts. Increased stringency is an ongoing topic of discussion and more stringent standards are usually associated with their beneficial environmental impact. Here we show that this is not necessarily the right direction with respect to reducing the climate impacts of aviation (as opposed to local air quality impacts) because of the tradeoff effects between reducing NOx emissions and increased fuel usage, along with a revised understanding of the radiative forcing effects of methane. Moreover, the predicted lower surface air pollution levels in the future will be beneficial for reducing the climate impact of aviation NOx emissions. Thus, further efforts leading to greater fuel efficiency, and therefore lower CO2 emissions, may be preferable to reducing NOx emissions in terms of aviation's climate impacts. 

Retracted: No

PubPeer comments:
 Figure 5 was pointed out to me by a reader. * Red boxes: Three bands in the bottom left P-P38 panel look similar to three bands in the bottom right IkBa panel. Could the authors proved higher resolution, uncropped blots here, please? ![file] ,
Assembling All-Solid-State Lithium-Sulfur Batteries with Li3N-Protected Anodes
Authors: Hatem Akbulut
Abdulkadir Kızılaslan
Journal: ChemPlusChem (2019)
Discipline: CHEMISTRY
Keywords: all-solid-state batteries; electrochemistry; electrodes; lithium nitride; solid electrolytes.
Affiliations: Metallurgy and Materials Science Department; Sakarya University; Esentepe Campus 54050 Sakarya Turkey

Abstract:  The construction of all-solid-state batteries is now easier after the successful synthesis of sulfur-based solid electrolytes with extremely high ionic conductivities. Utilizing lithium metal as the anode in these batteries requires a protective solid electrolyte layer to prevent corrosion due to the highly reactive nature of lithium. Li3 N coating on lithium metal is a promising way of preventing the degradation of the electrolyte during charge and discharge. In this study, utilization of a Li3 N-coated lithium anode and Li7 P3 S11 solid electrolyte are reported, where a quaternary reduced graphene oxide (rGO)/S/carbon black/Li7 P3 S11 composite is used as cathode in the assembled cell. Our results indicate that protecting the Li metal with a Li3 N coating does not affect the electrochemical characteristics of the cell and extends the cycle life of the battery. A cell assembled with a protective layer was shown to having 306 mAh g-1 capacity after 120 cycles at 160 mAh g-1 current density, whereas a cell without protective layer had a capacity of 260 mAh g-1 . 

Retracted: No

PubPeer comments:
 self plagiarism, same work from another published by the authors ! same figures and same data. http: www1.metalurji.org.tr immc2018 08_EMS 226.pdf ![file] ![file] ![file] , 
 Same data - figures are used in a previous publication !! , 
 # 2 seems to be right about the copy paste case; other data and images were also used and duplicated from the previous publication. , 
 the mentioned figures and data are below: ![file] , 
 ![file] ,
Increased infiltration of macrophages to radioresistant lung cancer cells contributes to the development of the additional resistance of tumor cells to the cytotoxic effects of NK cells
Authors: Peter C Keng
Xiang Xue
Mingjing Shen
Ying Tsai
Lijun Xu
Yuhchyau Chen
Rongying Zhu
Yongbing Chen
Soo Ok Lee
Journal: International journal of oncology (2018)
Discipline: CLINICAL MEDICINE
Keywords: macrophage infiltration; radioresistant lung tumors; natural killer cell-mediated immunity; conditioned medium; tumor-associated macrophage
Affiliations: Department of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA, Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China

Abstract:  In this study, in order to investigate the effects of increased macrophage infiltration to radioresistant lung tumors in regulating natural killer (NK) cell-mediated immunity, we examined whether the treatment of radioresistant cells with conditioned medium (CM) from phorbol myristate acetate (PMA)/interleukin (IL)-4 treated THP-1 cells (used as a tumor-associated macrophage source) leads to the development of the additional resistance of tumor cells to NK cell cytotoxicity. We found that the susceptibility of THP-1 CM-treated radioresistant cells to NK cell cytotoxicity was decreased compared to the non-treated cells. In addition, it was found that such a decreased susceptibility was associated with increased programmed death receptor ligand 1 (PD-L1) and decreased natural killer group 2D (NKG2D) ligand levels in tumor cells. We further discovered that the THP-1 cells secreted a high level of IL-6, and that blocking IL-6 action by the addition of a neutralizing antibody (Ab) for IL-6 into the THP-1 CM decreased the resistance of THP-1 CM-treated radioresistant cells to NK cell cytotoxicity. Moreover, we discovered that MEK/Erk was the most critical IL-6 downstream signaling pathway in triggering the THP-1 CM effect; thus, the addition of MEK/Erk inhibitor to THP-1 CM enhanced the susceptibility of the THP-1 CM-treated radioresistant cells to NK cell cytotoxicity. On the whole, the findings of this study suggest the existence of a malignant loop characterized by increased macrophage infiltration into radioresistant cells which, in turn, promotes the development of the additional resistance of these cells to NK cell cytotoxicity. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] ,
Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth
Authors: Wei Guo
Dingbo Shi
Wangbing Chen
Tiebang Kang
Wuguo Deng
Shusen Wang
Jingshu Wang
Huijuan Qiu
Xiaohong Zhang
Wenlin Huang
Yun Tian
Lingyi Fu
Xiangsheng Xiao
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Berberine; lung cancer; cell growth; apoptosis; signaling pathways
Affiliations: State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, China.

Abstract:  Berberine (BBR), an isoquinoline derivative alkaloid isolated from Chinese herbs, has a long history of uses for the treatment of multiple diseases, including cancers. However, the precise mechanisms of actions of BBR in human lung cancer cells remain unclear. In this study, we investigated the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells. Treatment with BBR promoted cell morphology change, inhibited cell migration, proliferation and colony formation, and induced cell apoptosis. Further molecular mechanism study showed that BBR simultaneously targeted multiple cell signaling pathways to inhibit NSCLC cell growth. Treatment with BBR inhibited AP-2α and AP-2β expression and abrogated their binding on hTERT promoters, thereby inhibiting hTERT expression. Knockdown of AP-2α and AP-2β by siRNA considerably augmented the BBR-mediated inhibition of cell growth. BBR also suppressed the nuclear translocation of p50/p65 NF-κB proteins and their binding to COX-2 promoter, causing inhibition of COX-2. BBR also downregulated HIF-1α and VEGF expression and inhibited Akt and ERK phosphorylation. Knockdown of HIF-1α by siRNA considerably augmented the BBR-mediated inhibition of cell growth. Moreover, BBR treatment triggered cytochrome-c release from mitochondrial inter-membrane space into cytosol, promoted cleavage of caspase and PARP, and affected expression of BAX and Bcl-2, thereby activating apoptotic pathway. Taken together, these results demonstrated that BBR inhibited NSCLC cell growth by simultaneously targeting AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF, PI3K/AKT, Raf/MEK/ERK and cytochrome-c/caspase signaling pathways. Our findings provide new insights into understanding the anticancer mechanisms of BBR in human lung cancer therapy. 

Retracted: No

PubPeer comments:
 Fig. 1B contains two images which appear to overlap, with obvious image manipulation. ![file] , 
 Fig. 6B contains a WB band which appears to be PS manipulated. ![file] ,
Lactotransferrin: a candidate tumor suppressor-Deficient expression in human nasopharyngeal carcinoma and inhibition of NPC cell proliferation by modulating the mitogen-activated protein kinase pathway
Authors: Yixin Tan
Wei Yi
Chen Huang
Yanhong Zhou
Shourong Shen
Minghua Wu
Wenling Zhang
Ke Tang
Xiaoling Li
Guiyuan Li
Wei Xiong
Lan Xiao
Xiayu Li
Zhaoyang Zeng
Li Cao
Journal: International Journal of Cancer (2008)
Discipline: CLINICAL MEDICINE
Keywords: Lactotransferrin; nasopharyngeal carcinoma; tumorogenesis; development; expression
Affiliations: Cancer Research Institute, Central South University, Changsha, Hunan 410078, People's Republic of China.

Abstract:  Lactotransferrin (LTF) has been shown to regulate tumorogenesis. However, little is known about the role of LTF in regulating the development of human nasopharyngeal carcinoma (NPC). The aim of our study was to investigate whether LTF could regulate the development of NPC by characterizing the pattern of LTF expression in human NPC tissues using cDNA and tissue microarrays. Loss of LTF expression was observed in a significantly higher frequency of NPC tissues compared to that in nontumor nasopharyngeal epithelial tissues. While 61.25% of NPC tissues at the T1/T2 stage were positive for LTF expression, only 40.82% of NPC at the T3/T4 stage were stained by anti-LTF. Similarly, 41.58% of NPC with local lymph node metastasis displayed LTF expression, a value significantly lower than the 46.36% in primary tumors (p &lt; 0.05). These findings suggest that LTF may negatively regulate the development and metastasis of NPC in vivo. Furthermore, overexpression of or treatment with LTF inhibited the proliferation of NPC cells and promoted cell cycle arrest at the G(0)/G(1) phase in vitro. While LTF treatment downregulated expression of cyclin D1 and phosphorylation of retinoblastoma protein (Rb), expression of p21 and p27 in 5-8F NPC cells was enhanced. Moreover, LTF treatment modulated the mitogen-activated protein kinase (MAPK) pathway, but did not affect p53 and STAT3 expression in 5-8F NPC cells. Thus LTF is likely to be a candidate tumor suppressor and downregulates the development of NPC by inhibiting NPC proliferation through induction of cell cycle arrest and modulation of the MAPK signaling pathway. Therefore, our findings provide new insights in understanding the mechanism(s) underlying the action of LTF in regulating the development of human NPC. 

Retracted: No

PubPeer comments:
 Do the authors still have access to the original data? I have some concerns about the possibility of repeated features in the Western blots in Figure 4a and 4b. I have illustrated two below as examples. *** ![file] *** ![file] ,