PReD-Bench/PRed-Bench huggingface dataset:
Enhanced susceptibility to apoptosis of oral squamous cell carcinoma cells subjected to combined treatment with anticancer drugs and phosphatidylinositol 3-kinase inhibitors
Authors: Masashi Hatori
Masayasu Iwase
Satoru Shintani
Daisuke Ito
Sayaka Takaoka
Sayaka Yoshiba
Yuji Kurihara
Makiko Uchid
Journal: International Journal of Oncology (2007)
Discipline: CLINICAL MEDICINE
Keywords: phosphatidylinositol 3-kinase (PI 3-K) inhibitors; apoptosis; anticancer drugs; cisplatin; 5-fluorouracil
Affiliations: Department of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Ota-ku, Tokyo 145-8515, Japan. 

Abstract:  The purpose of this study was to determine whether phosphatidylinositol 3-kinase (PI 3-K) inhibitors could modulate the apoptotic activity of the anticancer drugs cisplatin, 5-fluorouracil or docetaxel in an oral squamous cell carcinoma (OSCC) cell line, HSC-2. In preliminary experiments, cisplatin, 5-fluorouracil and docetaxel inhibited the proliferation of OSCC cells in a dose-dependent manner. We found that two PI 3-K inhibitors, wortmannin and LY294002, markedly suppressed the phosphorylation of Akt in OSCC cells. Treatment of OSCC cells with PI 3-K inhibitors significantly enhanced cisplatin-, 5-fluorouracil- or docetaxel-induced apoptosis. Caspase-3 and -9 inhibitors, but not a caspase-8 inhibitor, reduced anticancer drug-mediated apoptosis in PI 3-K inhibitor-treated OSCC cells, suggesting that the apoptotic pathway induced by the combination of anticancer drug therapy and PI 3-K inhibition may be functionally related to the intrinsic apoptotic pathway in OSCC cells. Expression of Bcl-2, cellular inhibitor of apoptosis protein-1 (cIAP-1), and X-linked IAP was down-regulated, and expression of Bax was up-regulated by PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated. We also found that Bad phosphorylation was down-regulated by PI 3-K inhibitors. These results suggested that inhibition of PI 3-K enhances the susceptibility of OSCC cells to anticancer drug-mediated apoptosis through regulation of expression and post-translational modification of both pro- and anti-apoptotic proteins. These findings could potentially lead to new strategies for improving the efficacy of anticancer drugs in OSCC cells. 

Retracted: No

PubPeer comments:
 This article shows the effect of PI 3-K inhibitors on phosphorylation of Akt in HSC-2 cells (Figure 1), on phosphorylation of Bad in HSC-2 cells (Figure 5), and on the expression of pro- and antiapoptotic proteins in HSC-2 cells (Figure 6). Several panels are duplicates of panels from other articles published by the same group ([Uchida_et_al_2007](http: pubpeer.com publications F5D53B6DE714FE0D8FBA554824458A#3) and [Takaoka_et_al_2007](http: pubpeer.com publications 43A433F2F37FCAAE0A10BD6DDC28A1#1)), where experiments, conditions and cell types were different. ![file] ,
Exosomal lncRNA 91H is associated with poor development in colorectal cancer by modifying HNRNPK expression
Authors: Bangshun He
Shukui Wang
Xiangxiang Liu
Chengbin Zhu
Zhenlin Nie
Pei Zhang
Tianyi Gao
Journal: Cancer Cell International (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Colorectal cancer (CRC); Exosomes; HNRNPK; Prognosis; lncRNA 91H.
Affiliations: 1Department of Clinical Laboratory, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006 Jiangsu China., 2Central Laboratory, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006 Jiangsu China.

Abstract:  Background: Exosomes mediated transfer of lncRNA 91H may play a critical role in the development of CRC. However, few studies have proved the mechanism. So we performed this study to deeply explore the biological functions of exosomal 91H in the development and progression of CRC. Methods: The association between lncRNA 91H and exosomes was detected in vitro and vivo. Then RNA pulldown and RIP were used to detect how lncRNA 91H affect CRC IGF2 express. At last, clinic pathological significance of exosomal 91H was evaluated by Cox proportional hazards model. Results: We found that serum lncRNA 91H expression was closely related to cancer exosomes in vitro and vivo which may enhance tumor-cell migration and invasion in tumor development by modifying HNRNPK expression. Then the clinic pathological significance of exosomal 91H was evaluated which demonstrated that CRC patients with high lncRNA 91H expression usually showed a higher risk in tumor recurrence and metastasis than patients with low lncRNA 91H expression (P &lt; 0.05). Conclusion: All these data suggested that exosomal lncRNA 91H enhancing CRC metastasis by modifying HNRNPK expression might be an early plasma-based biomarker for CRC recurrence or metastasis. Further large-scale studies are needed to confirm our findings. 

Retracted: No

PubPeer comments:
 Figure 5 (Migration) and Figure 6 (Invasion) appear to have an image that is repeated. *** ![file] ![file] , 
 Figure 4 appears to have two images which overlap. *** ![file] ,
Motif-driven interactions between RNA and PRC2 are rheostats that regulate transcription elongation
Authors: Michael Rosenberg
Jeannie T Lee
Eric Aeby
Attila Szanto
Roy Blum
Barry Kesner
Jean-Michel Garant
Journal: Nature Structural & Molecular Biology (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PRC2; RNA-binding complex; high-affinity RNA motifs; mutations; repressive function
Affiliations: Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA., Department of Genetics, Harvard Medical School, Boston, MA, USA., Canada's Michael Smith Genome Sciences Centre, Vancouver, British Columbia, Canada., RNA Group/Groupe ARN, Département de Biochimie, Faculté de Médecine et des Sciences de la Santé, Pavillon de Recherche Appliquée au Cancer, Université de Sherbrooke, Sherbrooke, Québec, Canada., Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA. ., Department of Genetics, Harvard Medical School, Boston, MA, USA. .

Abstract:  Although polycomb repressive complex 2 (PRC2) is now recognized as an RNA-binding complex, the full range of binding motifs and why PRC2-RNA complexes often associate with active genes have not been elucidated. Here, we identify high-affinity RNA motifs whose mutations weaken PRC2 binding and attenuate its repressive function in mouse embryonic stem cells. Interactions occur at promoter-proximal regions and frequently coincide with pausing of RNA polymerase II (POL-II). Surprisingly, while PRC2-associated nascent transcripts are highly expressed, ablating PRC2 further upregulates expression via loss of pausing and enhanced transcription elongation. Thus, PRC2-nascent RNA complexes operate as rheostats to fine-tune transcription by regulating transitions between pausing and elongation, explaining why PRC2-RNA complexes frequently occur within active genes. Nascent RNA also targets PRC2 in cis and downregulates neighboring genes. We propose a unifying model in which RNA specifically recruits PRC2 to repress genes through POL-II pausing and, more classically, trimethylation of histone H3 at Lys27. 

Retracted: No

PubPeer comments:
 https: twitter.com ReinbergDanny status 1411032588647600130 ,
5-fluorouracil loaded fibrinogen nanoparticles for cancer drug delivery applications
Authors: K P Chennazhi
N Sanoj Rejinold
S V Nair
M Muthunarayanan
R Jayakumar
Journal: International Journal of Biological Macromolecules (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 5-flurouracil; fibrinogen nanoparticles; drug delivery; cytotoxicity; cellular uptake
Affiliations: Amrita Centre for Nanosciences and Molecular Medicine, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham University, Kochi 682041, India.

Abstract:  In this study, 5-flurouracil loaded fibrinogen nanoparticles (5-FU-FNPs) were prepared by two step coacervation method using calcium chloride as cross-linker. The prepared nanoparticles were characterized using DLS, SEM, AFM, FT-IR, TG/DTA and XRD studies. Particle size of 5-FU-FNPs was found to be 150-200 nm. The loading efficiency (LE) and in vitro drug release was studied using UV spectrophotometer. The LE of FNPs was found to be ∼90%. The cytotoxicity studies showed 5-FU-FNPs were toxic to MCF7, PC3 and KB cells while they are comparatively non toxic to L929 cells. Cellular uptake of Rhodamine 123 conjugated 5-FU-FNPs was also studied. Cell uptake studies demonstrated that the nanoparticles are inside the cells. These results indicated that FNPs could be useful for cancer drug delivery. 

Retracted: No

PubPeer comments:
 Several papers by N. Sanoj Rejinold contain figures that look similar to each other. For sake of clarity, I will label these papers with letters. This is paper E. * Paper E: International journal of biological macromolecules 48, no. 1 (2011): 98-105. DOI: 10.1016 j.ijbiomac.2010.10.003 * Paper F: Carbohydrate polymers 84, no. 1 (2011): 407-416, DOI: 10.1016 j.carbpol.2010.11.056 Figure 2 of paper E and Figure 3 of paper F show different types of nanoparticles. Yet, their SEM photos look remarkably similar. Shown with pink boxes. ![file] , 
 Figure 6 of this paper shows MTT assay data obtained with 4 different cell types. Yet, all 4 graphs look remarkably similar. Relative heights and error bars are all unexpectedly similar. Shown with blue boxes. Could the authors please explain? ![file] , 
 Corrigendum published, [15 August 2019] . ------------------------------------ In the original manuscript Fig. 2c, SEM image of 5-FU loaded FNPs is incorrect. This mistake has been rectified and the corrected Fig. 2 is presented below. ![] Similarly, in the original manuscript, Fig. 6a is inadvertently repeated as Fig. 6bu2013d. We re-performed the entire experiments to rectify this mistake and provided the corrected Fig. 6au2013d is presented below. ![] These changes in the figures would not affect the conclusion from the respective figures nor the overall conclusion of the whole manuscript. The authors would like to apologise for any inconvenience caused. ,
Interleukin-36α axis is modulated in patients with primary Sjögren's syndrome
Authors: S Raimondo
G Guggino
A Rizzo
R Priori
R Alessandro
F Carubbi
C Alessandri
F Ciccia
A Accardo-Palumbo
G Valesini
R Giacomelli
G Triolo
Journal: Clinical and experimental immunology (2015)
Discipline: IMMUNOLOGY
Keywords: IL-36a; IL-38; IL36RA; Sjögren's syndrome; γδ T cells.
Affiliations: Dipartimento Biomedico di Medicina Interna e Specialistiche, Sezione di Reumatologia, Università di Palermo, Italy., Dipartimento di Oncoematologia, Azienda Ospedaliera Ospedali Riuniti Villa Sofia-Cervello, Sezione di Anatomia Patologica, Palermo, Italy., Dipartimento di Biopatologia e Biotecnologie Mediche e Forensi, Università di Palermo, Italy., UOC di Reumatologia, Dipartimento di Medicina Interna e Specialità Mediche, Sapienza Università degli Studi di Roma, Italy., UOC di Oculistica, Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università degli Studi di Palermo, Italy.

Abstract:  The aim of this study was to investigate the expression of the interleukin (IL)-36 axis in patients with primary Sjögren's syndrome (pSS). Blood and minor labial salivary glands (MSG) biopsies were obtained from 35 pSS and 20 non-Sjögren's syndrome patients (nSS) patients. Serum IL-36α was assayed by enzyme-linked immunosorbent assay (ELISA). IL-36α, IL-36R, IL-36RA, IL-38, IL-22, IL-17, IL-23p19 and expression in MSGs was assessed by reverse transcription-polymerase chain reaction (RT-PCR), and tissue IL-36α and IL-38 expression was also investigated by immunohistochemistry (IHC). αβ and γδ T cells and CD68(+) cells isolated from MSGs were also studied by flow cytometry and confocal microscopy analysis. IL-36α was over-expressed significantly in the serum and in the salivary glands of pSS. Salivary gland IL-36α expression was correlated with the expression levels of IL-17, IL-22 and IL-23p19. IL-38, that acts as inhibitor of IL-36α, was also up-regulated in pSS. αβ(+) CD3(+) T cells and CD68(+) cells were the major source of IL-36α in minor salivary glands of pSS. γδ T cells were not significantly expanded in the salivary glands of pSS but produced more IL-17, as their percentage correlated with the focus score. Higher expression of IL-36α and IL-36R was also demonstrated in γδ T cells isolated from pSS compared to controls. In this study we demonstrate that a significant increase in circulating and tissue levels of IL-36α occurs in pSS patients. 

Retracted: No

PubPeer comments:
 There are some odd unlikely similarities between two sets of panels in Figure 5 ![file] ,
Human SIRT6 promotes DNA end resection through CtIP deacetylation
Authors: Chunaram Choudhary
Stephen P Jackson
Abderrahmane Kaidi
Brian T Weinert
Journal: Science (2010)
Discipline: Multidisciplinary
Keywords: SIRT6; DNA end resection; DNA double-strand break repair; homologous recombination; replication protein A
Affiliations: Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.

Abstract:  SIRT6 belongs to the sirtuin family of protein lysine deacetylases, which regulate aging and genome stability. We found that human SIRT6 has a role in promoting DNA end resection, a crucial step in DNA double-strand break (DSB) repair by homologous recombination. SIRT6 depletion impaired the accumulation of replication protein A and single-stranded DNA at DNA damage sites, reduced rates of homologous recombination, and sensitized cells to DSB-inducing agents. We identified the DSB resection protein CtIP [C-terminal binding protein (CtBP) interacting protein] as a SIRT6 interaction partner and showed that SIRT6-dependent CtIP deacetylation promotes resection. A nonacetylatable CtIP mutant alleviated the effect of SIRT6 depletion on resection, thus identifying CtIP as a key substrate by which SIRT6 facilitates DSB processing and homologous recombination. These findings further clarify how SIRT6 promotes genome stability. 

Retracted: No

PubPeer comments:
 2019 retraction. https: science.sciencemag.org content 364 6437 247.1 After an investigation, the University of Cambridge has concluded that there was falsification of research data used in the Report u201cHuman SIRT6 promotes DNA end resection through CtIP deacetylationu201d (1), which was the subject of an Editorial Expression of Concern in September 2018 (2). The investigation concluded that the first author, Abderrahmane Kaidi, was responsible for the falsification of the data. In agreement with the recommendation of the investigation, the authors are retracting the Report. References and Notes u21b5A. Kaidi, B. T. Weinert, C. Choudhary, S. P. Jackson, Science 329, 1348 (2010). u21b5J. Berg, Science 361, 1322 (2018). , 
 https: retractionwatch.com 2019 04 11 authors-have-papers-in-nature-and-science-retracted-on-the-same-day ,
Antimetastatic effect of epigenetic drugs, hydralazine and valproic acid, in Ras-transformed NIH 3T3 cells
Authors: Alejandro García-Carrancá
Alfonso Dueñas-González
Catalina Trejo-Becerril
Enrique Pérez-Cárdenas
Elizabeth Langley
Guadalupe Domínguez-Gómez
José Chanona-Vilchis
Lucía Taja-Chayeb
Alma Chávez-Blanco
Journal: OncoTargets and Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: epigenetics; hydralazine; metastasis; ras; valproic acid.
Affiliations: Division of Basic Research, Instituto Nacional de Cancerología, Mexico City, Mexico., Department of Pathology, Instituto Nacional de Cancerología, Mexico City, Mexico., Unit of Biomedical Research on Cancer, Biomedical Research Institute, Universidad Nacional Autonoma de Mexico, Mexico City, Mexico, ., Unit of Biomedical Research on Cancer, Instituto Nacional de Cancerologia, Mexico City, Mexico, .

Abstract:  Introduction: Metastasis involves the accumulation of genetic and epigenetic alterations leading to activation of prometastatic genes and inactivation of antimetastatic genes. Among epigenetic alterations, DNA hypermethylation and histone hypoacetylation are the focus of intense translational research because their pharmacological inhibition has been shown to produce antineoplastic activity in a variety of experimental models. Aims: This study aimed to evaluate the antimetastatic effect of the DNA-methylation inhibitor, hydralazine, and the histone deacetylase inhibitor, valproic acid. Methods: NIH 3T3-Ras murine cells were treated with hydralazine and valproic acid to evaluate their effects upon cell proliferation, cell motility, chemotaxis, gelatinase activity, and gene expression. Lung metastases were developed by intravenous injection of NIH 3T3-Ras cells in BALB/c nu/nu mice and then treated with the drug combination. Results: Treatment induced a growth-inhibitory effect on NIH 3T3-Ras cells, showed a trend toward increased gelatinase activity of MMP2 and MMP9, and inhibited chemotaxis and cell motility. The combination led to a strong antimetastatic effect in lungs of nude mice. Conclusion: Hydralazine and valproic acid, two repositioned drugs as epigenetic agents, exhibit antimetastatic effects in vitro and in vivo and hold potential for cancer treatment. 

Retracted: No

PubPeer comments:
 Image in Figure 2C seems to have some repeated regions (red and magenta boxes). False color and full figure shown. *** ![file] *** ![file] *** ![file] ,
Anthelmintic pyrvinium pamoate blocks Wnt/β-catenin and induces apoptosis in multiple myeloma cells
Authors: Jingxuan Pan
Jun Zhong
Yingjie Zhu
Zhi Yu
Fang Xu
Yuhong Lu
Yangqiu Li
Journal: Oncology letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; multiple myeloma; synergism; β-catenin.
Affiliations: Jinan University Institute of Tumor Pharmacology, College of Pharmacy, Guangzhou, Guangdong 510632, P.R. China., Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510632, P.R. China.

Abstract:  Multiple myeloma (MM) is a malignancy of the bone marrow. The median survival time of patients with MM is only 5 years, with patients frequently experiencing relapse. Currently, there is no effective therapy for recurrent MM. The results of the present study indicated that pyrvinium pamoate (PP), a US Food and Drug Administration-approved oral anthelmintic drug, exhibited potent antitumor activity in MM cells in vitro. It is demonstrated that PP inhibited MM cell proliferation and mediated apoptosis. Notably, PP markedly promoted the degradation of β-catenin and abrogated its phosphorylation. PP triggered apoptosis in MM cells by inducing the release of cytochrome c and downregulating the expression of myeloid leukemia cell differentiation protein. In addition, PP effectively induced cell death in primary MM cells. In conclusion, PP may be a promising agent for the clinical treatment of MM. 

Retracted: No

PubPeer comments:
 Nick Coatsworth is a member of the Australian Health Principal Protection Committee, which is worth noting as a potential conflict of interest. The ICMJE form for disclosure of potential conflicts of interest asks  Are there other relationships or activities that readers could perceive to have influenced, or that give the appearance of potentially influencing, what you wrote in the submitted work? Given the topic of this paper I believe the answer to this question is yes and that the paper should be updated to reflect this in the interests of transparency. ,
IL-10 signaling via IL-10E1 is dependent on tyrosine phosphorylation in the IL-10R alpha chain in human primary prostate cancer cell lines
Authors: Min Wang
Youji Hu
Mark E Stearns
Journal: Oncogene (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Interleukin 10; IL-10E1; TIMP-1 gene; JAK1; TYK2
Affiliations: Department of Pathology and Laboratory, Drexel University College of Medicine, 15th and Vine Sts, Philadelphia, PA 19102-1192, USA. 

Abstract:  Interleukin 10 (IL-10) stimulates rapid nuclear translocation and binding of a 22 kDa protein, termed interleukin 10 enhancer 1 (IL-10E1), to a novel enhancer element (i.e. HTE-1) of the tissue inhibitor of metalloproteinase-1 (TIMP-1) gene to upregulate TIMP-1 expression. IL-10E1 signaling involves tyrosine phosphorylation of the IL-10R JAK1 (Janus kinase) and TYK2 (tyrosine kinase) receptor kinases and tyrosine phosphorylation of two tyrosine moieties (Y57 and Y62) of a LIM domain of the IL-10E1 protein. In this paper, the studies showed that two tyrosine residues (Tyr(446) and Tyr(496)) located in the cytoplasmic domain of the IL-10R alpha chain were required for receptor function, and for phosphorylation and activation of IL-10E1. Immunoprecipitation studies revealed that 12 amino-acid peptides encompassing either of these two tyrosine residues in phosphorylated form coprecipitated IL-10E1 and blocked ligand-dependent IL-10E1 phosphorylation in a cell-free system. In contrast, peptides containing serine substitutions for Tyr(446) and Tyr(496), and tyrosine-phosphorylated peptides containing Tyr(230) or Tyr(252/259) did not prevent IL-10E1 activation or signaling. To confirm these observations in vivo, fusion protein constructs were made between a modified form of green fluorescent protein or GFP and the intact IL-10E1 protein (IL-10E1-MmGFP) and n-terminal peptides of the IL-10E1 protein (i.e. nt-nls-MmGFP and mutant sequences identified as nt-nls mC61-MmGFP and nt-nls mY57/mY62-MmGFP peptides). Confocal microscopy revealed that IL-10 triggered transport to the nucleus of IL-10E1-MmGFP, nt-nls-MmGFP, and nt-nls mC61-MmGFP by 10-30 min in HPCA-10a (human prostrate cancer cells; derived from Gleason sum 10 tumor tissue) cells. IL-10 failed to induce nuclear translocation of the mY57/mY62-MmGFP peptides with point mutations of the two tyrosine groups. Coinjection of nt-nls-MmGFP with the IL-10R Tyr(446) and Tyr(496) amino-acid residues completely blocked ligand signaling. Coinjection of peptides containing either serine substitutions for Tyr(446) and Tyr(496) or Tyr(230) and Tyr(252/259) failed to block nt-nls-MmGFP signaling. The data demonstrate that IL-10E1 is directly recruited to the ligand-activated IL-10R by binding to specific phosphotyrosine groups which control tyrosine phosphorylation of the LIM domain of the IL-10E1 protein (i.e. Y57/Y62 groups) and IL-10E1 activation. 

Retracted: No

PubPeer comments:
 ![file] , 
 Identified by another reader. *** ![file] ,
Preparation of (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) nanocatalysts and application in sonocatalytic decomposition of ametryn in aqueous solution
Authors: Yidi Wang
Guanshu Li
Xuekai Dou
Jun Wang
Youtao Song
Yingying Huang
Hongbo Zhang
Chunsheng Wei
Journal: Ultrasonics Sonochemistry (2017)
Discipline: CHEMISTRY
Keywords: Ametryn; Sonocatalytic decomposition; TiO(2)-Ta(2)O(5) composite; Ultrasonic irradiation.
Affiliations: College of Environment, Liaoning University, Shenyang 110036, PR China., College of Chemistry, Liaoning University, Shenyang 110036, PR China., College of Chemistry, Liaoning University, Shenyang 110036, PR China; National Police University of China, Shenyang 110854, PR China., College of Environment, Liaoning University, Shenyang 110036, PR China; College of Chemistry, Liaoning University, Shenyang 110036, PR China. Electronic address: ., College of Environment, Liaoning University, Shenyang 110036, PR China. Electronic address: .

Abstract:  (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) powder, as a high effective sonocatalyst, was prepared using sol-gel and calcination method. Then it was characterized by X-ray diffractometer (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM) and energy dispersive X-ray spectroscopy (EDX). In order to evaluate the sonocatalytic activity of the prepared (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) powder, the sonocatalytic decomposition of ametryn was studied. In addition, some influencing factors such as different Ti/Ta molar ratios on the sonocatalytic activity of the prepared (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) powder, catalyst added amount with ultrasonic irradiation time and used times on the sonocatalytic decomposition efficiency were examined by using ion chromatogram determination. The experimental results showed that the best sonocatalytic decomposition ratio of ametryn were 77.50% based on the N atom calculation and 95.00% based on the S atom calculation, respectively, when the conditions of 10.00mg/L initial concentration, 1.00g/L prepared (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) powder (Ti/Ta=1.00:0.25 heat-treated at 550°C for 3.0h) added amount, 150min ultrasonic irradiation (40kHz frequency and 300W output power), 100mL total volume and 25-28°C temperature were adopted. Therefore, the (5.0%)Er3+:Y3Al5O12/Pt-(TiO2-Ta2O5) composite nanoparticles could be considered as an effective sonocatalyst for decomposition of ametryn in aqueous solution. 

Retracted: No

PubPeer comments:
 Although this is an older paper, could the authors please examine the marked similarities in two of the images in Figure 1? Are these similarities expected? *** ![file] ,
Differential morphology and homogeneity of tissue-engineered cartilage in hydrodynamic cultivation with transient exposure to insulin-like growth factor-1 and transforming growth factor-β1
Authors: Gilda A Barabino
Yueh-Hsun Yang
Journal: Tissue Engineering Part A (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: tissue-engineering; cartilage repair; chondrocytes; growth factors; mechanical stimuli
Affiliations: The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University , Atlanta, Georgia ., The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia.

Abstract:  Successful tissue-engineering strategies for cartilage repair must maximize the efficacy of chondrocytes within their limited life span. To that end, the combination of exogenous growth factors with mechanical stimuli holds promise for development of clinically relevant cartilage tissue substitutes. The current study aimed to determine whether incorporation of transient exposure to growth factors into a hydrodynamic bioreactor system can improve the functional maturation of tissue-engineered cartilage. Chondrocyte-seeded polyglycolic acid scaffolds were cultivated within a wavy-walled bioreactor that imparts fluid flow-induced shear stress for 4 weeks. Constructs were nourished with 100 ng/mL insulin-like growth factor-1 (IGF-1) or 10 ng/mL transforming growth factor-β1 (TGF-β1) either for the first 15 days of the culture (transient) or throughout the entire cultivation (continuous). Transiently treated constructs were found to exhibit better functional properties than continuously nourished constructs. The limited development of engineered tissues continuously stimulated by IGF-1 or TGF-β1 was related to massive growth factor leftovers in the environments that downregulated the expression of the associated receptors. Treatment with TGF-β1 eliminated the formation of a fibrous capsule at the construct periphery possibly through suppression of Smad3 phosphorylation, yielding constructs with greater homogeneity. Furthermore, TGF-β1 reversely regulated Smad2 and Smad3 pathways in articular chondrocytes under hydrodynamic stimuli partially via Smad7. Collectively, transient exposure to growth factors is likely to maintain chondrocyte homeostasis, and thus promotes their anabolic activities under hydrodynamic stimuli. The present work suggests that robust hydrodynamically engineered neocartilage with a reduced fibrotic response and enhanced tissue homogeneity can be achieved through optimization of growth factor supplementation protocols and potentially through manipulation of intracellular signals such as Smad. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] ,
Induction of p21 by p53 following DNA damage inhibits both Cdk4 and Cdk2 activities
Authors: Ryuji Kobayashi
Ruoning Wang
Guangan He
John Koomen
Zaifeng Huang
Abdul R Khokhar
Jian Kuang
Zahid H Siddik
Journal: Oncogene (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA damage; p53-p21 pathway; G(1)-phase arrest; Cdk4 inhibition; Diaminocyclohexane(trans-diacetato)(dichloro) platinum(IV) (DAP)

Abstract:  DNA damage often activates the p53-p21 pathway and causes G(1)-phase arrest in mammalian cells. Although there is ample evidence that p21 induction by p53 leads to Cdk2 inhibition, it is unclear whether this checkpoint event also leads to Cdk4 inhibition. Diaminocyclohexane(trans-diacetato)(dichloro) platinum(IV) (DAP), a platinum-based coordination complex, is a DNA-damaging agent that is effective against a variety of tumor cells resistant to the parental drug cisplatin. Our previous studies established that treatment of human cancer cells with low effective concentrations of DAP specifically activates the G(1)-phase checkpoint and simultaneously inhibit Cdk4 and Cdk2 activities. Here we demonstrate that DAP treatment of human cancer cells activates the p53-p21 pathway without activating other known mechanisms that inhibit Cdk4 and Cdk2 activities. The induced p21 binds to both the Cdk4/cyclin D and Cdk2/cyclin E complexes and inhibits both of their kinase activities. Conversely, inhibition of p21 induction by cycloheximide or by p21 gene deletion prevents DAP-induced inhibition of Cdk4 and Cdk2 activities. Attenuated p53 expression and p21 induction also eliminates DAP-induced G(1)-phase arrest and inhibition of Cdk4 and Cdk2 activities. Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities. 

Retracted: No

PubPeer comments:
 Figure 8f. Much more similar than you would expect. https: imgur.com FhRz9II ,
mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling
Authors: Neal Rosen
Maurizio Scaltriti
Elizabeth Moskatel
Sarat Chandarlapaty
Vanessa S Rodrik-Outmezguine
Sylvie Guichard
Nen C Pagano
Poulikos I Poulikakos
José Baselga
Journal: Cancer Discovery (2011)
Discipline: CLINICAL MEDICINE
Keywords: AKT regulation; feedback; mTOR kinase.
Affiliations: Program in Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.

Abstract:  mTOR kinase inhibitors block mTORC1 and mTORC2 and thus do not cause the mTORC2 activation of AKT observed with rapamycin. We now show, however, that these drugs have a biphasic effect on AKT. Inhibition of mTORC2 leads to AKT serine 473 (S473) dephosphorylation and a rapid but transient inhibition of AKT T308 phosphorylation and AKT signaling. However, inhibition of mTOR kinase also relieves feedback inhibition of receptor tyrosine kinases (RTK), leading to subsequent phosphoinositide 3-kinase activation and rephosphorylation of AKT T308 sufficient to reactivate AKT activity and signaling. Thus, catalytic inhibition of mTOR kinase leads to a new steady state characterized by profound suppression of mTORC1 and accumulation of activated AKT phosphorylated on T308, but not S473. Combined inhibition of mTOR kinase and the induced RTKs fully abolishes AKT signaling and results in substantial cell death and tumor regression in vivo. These findings reveal the adaptive capabilities of oncogenic signaling networks and the limitations of monotherapy for inhibiting feedback-regulated pathways. Significance: The results of this study show the adaptive capabilities of oncogenic signaling networks, as AKT signaling becomes reactivated through a feedback-induced AKT species phosphorylated on T308 but lacking S473. The addition of RTK inhibitors can prevent this reactivation of AKT signaling and cause profound cell death and tumor regression in vivo, highlighting the possible need for combinatorial approaches to block feedback-regulated pathways. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than expected. ![file] ,
Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expression
Authors: Robert E White
Jade Yee
Emma Anderton
Martin J Allday
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Epstein-Barr virus (EBV); Burkitt's lymphoma; apoptosis; B cells; latency-associated nuclear proteins
Affiliations: Section of Virology, Division of Infectious Diseases, Faculty of Medicine, Imperial College London, London, United Kingdom.

Abstract:  Latent Epstein-Barr virus (EBV) has been shown to protect Burkitt's lymphoma-derived B cells from apoptosis induced by agents that cause damage to DNA, in the context of mutant p53. This protection requires expression of the latency-associated nuclear proteins EBNA3A and EBNA3C and correlates with their ability to cooperate in the repression of the gene encoding the pro-apoptotic, BH3-only protein BIM. Here we confirm that latent EBV in B cells also inhibits apoptosis induced by two other agents--ionomycin and staurosporine--and show that these act by a distinct pathway that involves a p53-independent increase in expression of another pro-apoptotic, BH3-only protein, NOXA. Analyses employing a variety of B cells infected with naturally occurring EBV or B95.8 EBV-BAC recombinant mutants indicated that the block to NOXA induction does not depend on the well-characterized viral latency-associated genes (EBNAs 1, 2, 3A, 3B, 3C, the LMPs or the EBERs) or expression of BIM. Regulation of NOXA was shown to be at least partly at the level of mRNA and the requirement for NOXA to induce cell death in this context was demonstrated by NOXA-specific shRNA-mediated depletion experiments. Although recombinant EBV with a deletion removing the BHRF1 locus--that encodes the BCL2-homologue BHRF1 and three microRNAs--partially abrogates protection against ionomycin and staurosporine, the deletion has no effect on the EBV-mediated block to NOXA accumulation. 

Retracted: No

PubPeer comments:
 The tissue samples for Patient 1 and Patient 2 shown in Figure 1A seem unexpectedly similar. *** ![file] , 
 #1 Dear Actinopolyspora Biskrensis, We have already noticed this problem. As you can see, we put the adjacent tissue of patient1 in Figure 1A and the adjacent tissue of patient2 in reverse. We will contact the editorial department publications as soon as possible. thank you so much for your suggestion. ,
Retraction: Chen, J. et al. Computational Fluid Dynamics Modeling of the Catalytic Partial Oxidation of Methane in Microchannel Reactors for Synthesis Gas Production. Processes 2018, 6, 83
Authors: Tomas Pieler
Annette Borchers
Journal: Processes (2019)
Discipline: CHEMISTRY
Keywords: Xenopus embryos; pluripotent cells; organogenesis; human embryonic stem cells; animal cap cells

Abstract:  Xenopus embryos provide a rich source of pluripotent cells that can be differentiated into functional organs. Since the molecular principles of vertebrate organogenesis appear to be conserved between Xenopus and mammals, this system can provide useful guidelines for the directional manipulation of human embryonic stem cells. Pluripotent Xenopus cells can be easily isolated from the animal pole of blastula stage Xenopus embryos. These so called "animal cap" cells represent prospective ectodermal cells, but give rise to endodermal, mesodermal and neuro-ectodermal derivatives if treated with the appropriate factors. These factors include evolutionary conserved modulators of the key developmental signal transduction pathways that can be supplied either by mRNA microinjection or direct application of recombinant proteins. This relatively simple system has added to our understanding of pancreas, liver, kidney, eye and heart development. In particular, recent studies have used animal cap cells to generate ectopic eyes and hearts, setting the stage for future work aimed at programming pluripotent cells for regenerative medicine. 

Retracted: No

PubPeer comments:
 **RETRACTED** **by Processes Editorial Office:**  We have become aware that figures, tables, experimental data, and a whole paragraph in the results and discussion section of the published article [1] are identical to a previously published paper by the same authors [2]. While the authors claimed that the work was sufficiently different to the previously published work, our editorial board disagreed, and we have therefore decided to retract the paper. Despite low levels of textual overlap, the work is essentially the same as that previously reported. MDPI is a member of the Committee on Publication Ethics and takes the responsibility to enforce strict ethical policies and standards very seriously. To ensure the addition of only high quality scientific works to the field of scholarly publication, [1] is retracted and shall be marked accordingly. We apologize to the readership of Processes for any inconvenience caused. We note that two other papers by the same author are being retracted for similar reasons [3,4]. ![file] ,
Activated protein C protects myocardium via activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart
Authors: Song Li
Yan Zhang
Xiao-Hong Tong
Zhao-Qi Liu
Jia-Wang Ding
Jian Yang
Jun Yang
Li Li
Journal: Journal of Korean Medical Science (2010)
Discipline: CLINICAL MEDICINE
Keywords: Activated Protein C; Cardioprotection; Reperfusion Injury, ERK1/2; bcl-2-Associated X Protein.
Affiliations: Department of Cardiology, the First College of Clinical Medical Science, China Three Gorges University, Yichang, Hubei, China., The Institute of Molecular Biology, China Three Gorges University, Yichang, Hubei, China., Department of Cardiology, Yichang Central People's Hospital, Yichang, Hubei, China.

Abstract:  Activated protein C (APC) is known to be beneficial on ischemia reperfusion injury in myocardium. However, the protection mechanism of APC is not fully understood. The purpose of this study was to investigate the effects and possible mechanisms of APC on myocardial ischemic damage. Artificially ventilated anaesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 hr of reperfusion. Rats were randomly divided into four groups; Sham, I/R, APC preconditioning and postconditioning group. Myocardial infarct size, apoptosis index, the phosphorylation of ERK1/2, Bcl-2, Bax and cytochrome c genes and proteins were assessed. In APC-administrated rat hearts, regardless of the timing of administration, infarct size was consistently reduced compared to ischemia/reperfusion (I/R) rats. APC improved the expression of ERK1/2 and anti-apoptotic protein Bcl-2 which were significantly reduced in the I/R rats. APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c. These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration. 

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. ,
Aquasomes--a nanoparticulate approach for the delivery of antigen
Authors: Amit K Goyal
Suresh Prasad Vyas
Neeraj Mishra
Shailja Tiwari
Bhuvaneshwar Vaidya
Kapil Khatri
Abhinav Mehta
Journal: Drug development and industrial pharmacy (2008)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: vaccine research; aquasomes; hydroxyapatite; adjuvanticity; polyhydroxyl oligomers
Affiliations: Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences, Dr. Harisingh Gour Vishwavidyalaya, Sagar, Madhya Pradesh, India.

Abstract:  The development of compound that enhances immune responses to recombinant or synthetic epitopes is of considerable importance in vaccine research. Of the many different types of immunopotentiating compounds that have been researched, aquasomes are of considerable promise, because of their potency and adjuvanticity. Aquasomes were prepared by self-assembling of hydroxyapatite by co-precipitation method and thereafter preliminary coated with polyhydroxyl oligomers (cellobiose and trehalose) and subsequently adsorbed with bovine serum albumin (BSA) as a model antigen. The prepared systems were characterized for size, shape, antigen-loading efficiency, in vitro antigen stability, and in vivo performance. BSA-immobilized aquasomes were around 200 nm in diameter and spherical in shape and had approximately 20-30% BSA-loading efficiency. The immunological activity of the formulated aquasomes was compared with plain BSA and better results were observed. Studies also indicated that aquasome formulations could elicit combined T-helper 1 (Th1) and Th2 immune response. 

Retracted: No

PubPeer comments:
 Fig 1A:  Electron microphotograph of different formulations: **(A) transmission electron microscope (TEM) image plain hydroxyapatite**; (B) TEM image of cellobiose-coated aquasomes; (C) TEM image of trehalose-coated aquasomes. ![file] Fig 1 from [Goyal et al (2009)] .  Characterization of prepared HA:...(b) TEM image of prepared ceramic decoy with MSP-119 (i) **HA (without spray dried)**, (ii) HAS (spray dried); (c) XRD analysis of spraydried Ha; (d) EDAX analysis of spray-dried HA. ![file] It is unclear whether the marked panel represents particles of plain pulvverised hydroxyapatite, or of hyoxyapatite synthesised without spray-drying and then coated with MSP-119. ,
Deubiquitinating enzyme CYLD regulates the peripheral development and naive phenotype maintenance of B cells
Authors: Minying Zhang
Wei Jin
Shao-Cong Sun
William R Reiley
Xuefeng Wu
Andrew J Lee
Ato Wright
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Deubiquitinating enzymes; DUB; CYLD; B cells; lymphoid organ
Affiliations: Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

Abstract:  Deubiquitinating enzymes (DUB) form a family of cysteine proteases that digests ubiquitin chains and reverses the process of protein ubiquitination. Despite the identification of a large number of DUBs, their physiological functions remain poorly defined. Here we provide genetic evidence that CYLD, a recently identified DUB, plays a crucial role in regulating the peripheral development and activation of B cells. Disruption of the CYLD gene in mice results in B cell hyperplasia and lymphoid organ enlargement. The CYLD-deficient B cells display surface markers indicative of spontaneous activation and are hyperproliferative upon in vitro stimulation. When challenged with antigens, the CYLD(-/-) mice develop exacerbated lymphoid organ abnormalities and abnormal B cell responses. Although the loss of CYLD has only a minor effect on B cell development in bone marrow, this genetic deficiency disrupts the balance of peripheral B cell populations with a significant increase in marginal zone B cells. In keeping with these functional abnormalities, the CYLD(-/-) B cells exhibit constitutive activation of the transcription factor NF-kappaB due to spontaneous activation of IkappaB kinase beta and degradation of the NF-kappaB inhibitor IkappaBalpha. These findings demonstrate a critical role for CYLD in regulating the basal activity of NF-kappaB and maintaining the naive phenotype and proper activation of B cells. 

Retracted: No

PubPeer comments:
 The authors are requested to clarify which isomer of tartaric acid was used by them in the experiment. Was it the D isomer or the L-isomer or DL or meso-tartaric acid. The identical powder pattern of the pure and TA influenced ADP crystal probably indicates that the more soluble tartaric acid remained in solution and the ADP crystal fractionally crystallized. This appears to be one more doping claim by the Shkir group. , 
 What are the new results in this paper which were not earlier reported by Shkir et al in an earlier paper titled,  Study of pure and l-tartaric acid doped ammonium dihydrogen phosphate single crystals: A novel nonlinear optical non-centrosymmetric crystal published in Materials Chemistry and Physics, 144, (2014) 293-300 https: www.sciencedirect.com science article pii S0254058413009127 , 
 In the abstract authors write,  *The TA influenced ADP single crystal has been grown by slow solvent evaporation method at room temperature.*  Authors are requested to explain what a so-called TA influenced ADP single crystal means and if it is same or different from that of a tartaric acid doped ADP crystal. ,
Expression of Japanese encephalitis virus envelope protein in transgenic tobacco plants
Authors: M Z Abdin
Mohan Babu Appaiahgari
Sudhanshu Vrati
K C Bansal
Journal: Journal of virological methods (2009)
Discipline: MICROBIOLOGY
Keywords: virus envelope protein; Japanese encephalitis virus; vaccine antigen; prM protein; transgenic tobacco plants
Affiliations: National Institute of Immunology and Vaccine and Infectious Disease Research Center, THSTI, New Delhi 110067, India.

Abstract:  The virus envelope (E) protein of Japanese encephalitis virus induces virus-neutralizing antibodies and is therefore a potential vaccine antigen. In a mammalian system, co-expression of another viral structural protein prM is necessary for proper expression and folding of E protein. Transgenic tobacco plants were produced carrying JEV cDNA encoding prM and E proteins under the control of the CaMV 35S promoter. E protein, however, was not detectable in these plants. In vitro translation studies showed that the presence of the prM sequence inhibited transgene expression in the plant system. Accordingly, JEV E protein could be expressed in transgenic tobacco plants only without the prM protein. 

Retracted: No

PubPeer comments:
 ![file] ,