PReD-Bench/PRed-Bench huggingface dataset:
Drug-resistant breast carcinoma (MCF-7) cells are paradoxically sensitive to apoptosis
Authors: Kapil Mehta
Sen Pathak
Marina Konopleva
Asha S Multani
Michael Andreeff
Jack S K Chen
Journal: Journal of Cellular Physiology (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: tissue transglutaminase; caspase-3; drug-resistant breast carcinoma; MCF-7/DOX cells; apoptotic stimuli
Affiliations: Department of Bioimmunotherapy, The University of Texas, M.D. Anderson Cancer Center, Houston, Texas 77030, USA.

Abstract:  The purpose of this study was to determine whether expression of tissue transglutaminase (TG2) and caspase-3 proteins in drug-resistant breast carcinoma MCF-7/DOX cells would render these cells selectively susceptible to apoptotic stimuli. Despite high resistance to multidrug resistance (MDR)-related drug, doxorubicin (&gt; or =150-fold), the MCF-7/DOX cells were extremely sensitive to apoptotic stimuli. Thus, calcium ionophore, A23187 (A23187) and the protein kinase C inhibitor staurosporine (STS) each induced rapid and time-dependent apoptosis in MCF-7/DOX cells. The apoptosis induced by either agent was accompanied by caspase-3 activation and other downstream changes that are typical of cells undergoing apoptosis. The alterations upstream of caspase-3 activation, however, such as loss in mitochondrial membrane potential (DeltaPsi), release of cytochrome c, and activation of caspase-8, and caspase-9, were detected only in STS-treated cells. The A12387 failed to induce any of the caspase-3 upstream changes, implying that A23187-induced apoptosis may utilize one or more novel upstream pathways leading to the activation of caspase 3. In summary, these data demonstrate that MCF-7/DOX cells are much more sensitive to apoptotic stimuli than previously thought and that A23187-induced apoptosis may involve some novel, yet unidentified, upstream pathway that leads to the activation of caspase-3 and other downstream events. 

Retracted: No

PubPeer comments:
 Figure 4C. https: imgur.com FllYIsv ,
MicroRNA-137 is downregulated in human osteosarcoma and regulates cell proliferation and migration through targeting FXYD6
Authors: Yu-Xue Wang
Hong-Yan Zhang
Zheng-Min Li
Wen-Bo Wang
Journal: Journal of Drug Targeting (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA 137; osteosarcoma; regulation; in vitro; in vivo

Abstract:  Background: In this work, we investigated the functional role of microRNA 137 (miR-137) in regulating osteosarcoma both in vitro and in vivo. Methods: Quantitative RT-PCR was used to examine the gene expressions of miR-137 in osteosarcoma cell lines and osteosarcoma tumors. 143B and Saos-2 cells were infected with lentivirus expressing miR-137 mimics (miR-137-mimic) to ectopically upregulate miR-137. In vitro cancer proliferation and migration were examined by MTT assay and transwell assay, respectively. Viral infected Saos-2 cells were also subcutaneously inoculated into null mice to evaluate the effect of miR-137 upregulation on in vivo tumor growth. The interaction between miR-137 and its downstream target, FXYD6, was evaluated by dual-luciferase reporter assay and quantitative real-time PCR. FXYD6 was then subsequently upregulated in osteosarcoma cells to evaluate its effect on miR-137 regulation in osteosarcoma. Results: We found that miR-137 was significantly downregulated in both osteosarcoma cell lines and osteosarcoma tumors. Lentiviral infection of miR-137-mimic upregulated miR-137 gene expression, reduced in vitro proliferation and migration and inhibited in vivo osteosarcoma tumor growth. FXYD6 was verified to be directly interacting with miR-137, and its subsequent upregulation reversed the inhibitory effect of miR-137 upregulation in osteosarcoma. Conclusion: We revealed novel functional role of miR-137 in osteosarcoma regulation, likely through FXYD6 binding. 

Retracted: No

PubPeer comments:
 After taking a deeper look at Figure 4E and F, I am afraid that this article is a falsification. Parts of the two micrographs in Figure 4E appear in the two micrographs in Figure 4F. ![file] , 
 #1 Fig 2B: ![file] Fig 2D: ![file] , 
 Fig 4E is not very subtle. ![file] ,
Tbx1 Regulates Proliferation and Differentiation of Multipotent Heart Progenitors
Authors: Antonio Baldini
Li Chen
Susan Tang
Filomena Gabriella Fulcoli
Journal: Circulation Research (2009)
Discipline: CLINICAL MEDICINE
Keywords: TBX1; T-box transcription factor; DiGeorge syndrome; heart development; cardiac progenitor cells
Affiliations: Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA., From the Institute of Biosciences and Technology (L.C., S.T., A.B.), Texas A&amp;M University Health Science Center, Houston; Program in Cardiovascular Sciences (L.C.), Baylor College of Medicine, Houston, Tex; University Federico II (A.B.), Naples, Italy; Telethon Institute of Genetics and Medicine (A.B.), Naples, Italy; and Institute of Genetics and Biophysics (F.G.F., A.B.), Consiglio Nazionale delle Ricerche, Naples, Italy.

Abstract:  Rationale: TBX1 encodes a T-box transcription factor implicated in DiGeorge syndrome, which affects the development of many organs, including the heart. Loss of Tbx1 results into hypoplasia of heart regions derived from the second heart field, a population of cardiac progenitors cells (CPCs). Thus, we hypothesized that Tbx1 is an important player in the biology of CPCs. Objective: We asked whether Tbx1 is expressed in multipotent CPCs and, if so, what role it may play in them. Methods and results: We used clonal analysis of Tbx1-expressing cells and loss and gain of function models, in vivo and in vitro, to define the role of Tbx1 in CPCs. We found that Tbx1 is expressed in multipotent heart progenitors that, in clonal assays, can give rise to 3 heart lineages expressing endothelial, smooth muscle and cardiomyocyte markers. In multipotent cells, Tbx1 stimulates proliferation, explaining why Tbx1(-/-) embryos have reduced proliferation in the second heart field. In this population, Tbx1 is expressed while cells are undifferentiated and it disappears with the onset of muscle markers. Loss of Tbx1 results in premature differentiation, whereas gain results in reduced differentiation in vivo. We found that Tbx1 binds serum response factor, a master regulator of muscle differentiation, and negatively regulates its level. Conclusions: The Tbx1 protein marks CPCs, supports their proliferation, and inhibits their differentiation. We propose that Tbx1 is a key regulator of CPC homeostasis as it modulates positively their proliferation and negatively their differentiation. 

Retracted: No

PubPeer comments:
 Figure 6G. Much more similar than you would expect. https: imgur.com d6xaSNf ,
Functional characterization of CD4+ T cells in aplastic anemia
Authors: Benedetta Costantini
Sufyan Al-Khan
Azim Mohamedali
Caroline Veen
Pilar Perez Abellan
Jie Jiang
Austin G Kulasekararaj
Farzin Farzaneh
Syed A Mian
Nana Benson-Quarm
Shahram Kordasti
Judith Marsh
Alexander Smith
Thomas Seidl
Ghulam J Mufti
Journal: Blood (2012)
Discipline: CLINICAL MEDICINE
Keywords: CD4(+) T cells; aplastic anemia; Th1 cells; Th2 cells; Tregs
Affiliations: Department of Haematological Medicine, King's College London, Rayne Institute, 123 Coldharbour Lane, London, United Kingdom., Department of Haematological Medicine, King's College London, London, United Kingdom;, Haematology Department, King's College Hospital, London, United Kingdom; and, Universitè Politecinica delle Marche, Clinica di Ematologia, Ancona, Italy

Abstract:  The role of CD4(+) T cells in the pathogenesis of aplastic anemia (AA) is not well characterized. We investigate CD4(+) T-cell subsets in AA. Sixty-three patients with acquired AA were studied. Th1 and Th2 cells were significantly higher in AA patients than in healthy donors (HDs; P = .03 and P = .006). Tregs were significantly lower in patients with severe AA than in HDs (P &lt; .001) and patients with non-severe AA (P = .01). Th17 cells were increased in severe AA (P = .02) but normal in non-severe AA. Activated and resting Tregs were reduced in AA (P = .004; P = .01), whereas cytokine-secreting non-Tregs were increased (P = .003). Tregs from AA patients were unable to suppress normal effector T cells. In contrast, AA effector T cells were suppressible by Tregs from HDs. Th1 clonality in AA, investigated by high-throughput sequencing, was greater than in HDs (P = .03). Our results confirm that Th1 and Th2 cells are expanded and Tregs are functionally abnormal in AA. The clonally restricted expansion of Th1 cells is most likely to be antigen-driven, and induces an inflammatory environment, that exacerbate the functional impairment of Tregs, which are reduced in number. 

Retracted: No

PubPeer comments:
 ![file] , 
 ERRATUM| AUGUST 27, 2020 In Figure 6E on page 2040, the wrong image is shown for spectratype IV. The corrected Figure 6E is shown below. The error does not change the interpretation of the findings of the study. ![file] ,
Pro-apoptotic miRNA-128-2 modulates ABCA1, ABCG1 and RXRα expression and cholesterol homeostasis
Authors: N Saini
R Singh
S Khanna
A Agrawal
Y K Adlakha
V P Singh
Journal: Cell death & disease (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cholesterol homeostasis; microRNA-128-2; ABCA1; ABCG1; SREBP
Affiliations: Functional Genomics Unit, CSIR-Institute of Genomics and Integrative Biology (IGIB), Council of Scientific and Industrial Research (CSIR), Delhi, India.

Abstract:  Aberrant regulation of cholesterol homeostasis is associated with obesity as well as multiple types of cancer. However, the mechanism behind these is largely missing. Here, we show that microRNA (miRNA)-128-2 is not only a pro-apoptotic microRNA but it also alters the expression of genes involved in cellular cholesterol homeostasis. Cholesterol efflux via ATP-binding cassette transporters (ABCA1 and ABCG1) is a mechanism for cells to eliminate excess cholesterol and prevent cellular cholesterol accumulation. The regulation of these pathways is complex with transcriptional regulation by sterol-regulatory element-binding protein (SREBP) and liver X receptor/retinoid X receptor (RXR) transcription factors but poorly understood at the post-transcriptional levels. MiR-128-2 increases the expression of SREBP2 and decreases the expression of SREBP1 in HepG2, MCF7 and HEK293T cells independent of sirtuin 1 (SIRT1) status. MiR-128-2 inhibits the expression of ABCA1, ABCG1 and RXRα directly through a miR-128-2-binding site within their respective 3'untranslated regions. The administration of miR-128-2 leads to decline in the protein and mRNA levels of ABCA1, ABCG1 and RXRα. Conversely, anti-miRNA treatment leads to increased ABCA1, ABCG1 and RXRα expression. The inverse correlation between miR-128-2 and its targets viz. ABCA1 and ABCG1 was also established during high-fat diet in different mice tissues. Our data show that cholesterol efflux is attenuated by miR-128-2 overexpression and, conversely, stimulated by miR-128-2 silencing. Further, we also observed the induction of ER stress response by miR-128-2. In this study, we provide the first evidence of miR-128-2 to be a new regulator of cholesterol homeostasis. Our study shows dual role of miR-128-2, as a pro-apoptotic molecule as well as a regulator of cholesterol homeostasis. 

Retracted: No

PubPeer comments:
 ![](http: ) ![file] , 
 Thankyou for pointing out . Sorry for the inadvertant mistake.must have happened during compiling revisions etc as both the manuscripts were being communicated simultaneously. Will check with first aithor and do the needful ,
In vitro and in vivo inhibition of epidermal growth factor receptor-tyrosine kinase pathway by photodynamic therapy
Authors: K Kalka
N Ahmad
H Mukhtar
Journal: Oncogene (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PDT; skin cancer; photosensitizing compound; WAF1/p21-cyclins; Rb/E2F-DP machinery
Affiliations: Department of Dermatology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA.

Abstract:  PDT, a new therapeutic procedure for the management of many malignant conditions including skin cancer, involves the administration of a photosensitizing compound followed by illumination of the lesion with visible light. We earlier showed an involvement of: (i) WAF1/p21-cyclins (D1 and E)-cdk (2 and 6) network; and (ii) Rb/E2F-DP machinery during silicon phthalocyanine (Pc4)-PDT-mediated cell cycle dysregulation and apoptosis of human epidermoid carcinoma (A431) cells. Here, we investigated the involvement of EGFR-pathway during antiproliferative responses of Pc4-PDT in A431 cells and during ablation of murine skin papillomas. Pc4-PDT of A431 cells was found to result in a time-dependent down-modulation of the protein expression and phosphorylation of EGFR and Shc (an immediate downstream molecule in EGFR-pathway), during progressive increase in apoptotic response. To establish the relevance of these in vitro findings to in vivo situations, we subjected chemically- as well as ultraviolet B radiation-induced squamous papillomas in SENCAR and SKH-1 hairless mice, respectively, to Pc4-PDT, and assessed its effect on EGFR-pathway during ablation of these tumors. Pc4-PDT was found to result in a time-dependent: (i) inhibition of protein expressions of EGFR; and (ii) tyrosine phosphorylation of EGFR and Shc; and (iii) induction of apoptosis, during the regression of these tumors. These data suggest the involvement of EGFR-pathway during the antiproliferative effects of PDT. It is tempting to speculate that inhibitors of EGFR could enhance the therapeutic efficacy of PDT. 

Retracted: No

PubPeer comments:
 Figure 1. Much more similar than expected. https: imgur.com uV7Lxlk , 
 Figure 2. Much more similar than expected. https: imgur.com 09UvVfW ,
Human homologue of SETA binding protein 1 interacts with cathepsin B and participates in TNF-Induced apoptosis in ovarian cancer cells
Authors: Hong Lu
Jian-Ping Liu
Han-Ying Yuan
Qian Guo
Yu-Yang Li
Nan-Song Liu
Journal: Molecular and Cellular Biochemistry (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: cathepsin B; apoptosis; hSB1; TNF; ovarian cancer cells
Affiliations: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, PR China.

Abstract:  Lysosomal cysteine protease cathepsin B has been reported to play an important role in apoptosis of many different cancer cells, but the regulation of cathepsin B in apoptosis is poorly understood. Human homologue of SETA binding protein 1 (hSB1) was identified to interact with cathepsin B by yeast-two hybrid method, and the interaction was confirmed in vitro GST pull-down assay and in vivo coimmunoprecipitation experiment. hSB1 was co-localized with cathepsin B in cellular lysosomes. Our previous study has shown that TNF can induce ovarian cancer cells OV-90 apoptosis and the apoptosis process is cathepsin B-depended. Here we provide evidence that overexpression of cathepsin B-interacting protein hSB1 could suppress TNF-triggered apoptosis in OV-90 cells, but has no effect on cellular cathepsin B activity. hSB1 may function as a regulator of cathepsin B-mediated apoptosis. 

Retracted: No

PubPeer comments:
 Figure 1. * Red boxes: a set of lanes in the GAPDH panel appears to be visible twice. Reported to the journal in October 2015, with a friendly reminder in 2017, but nothing has been done as of today. ![file] ,
A decrease in remodeling accounts for the accumulation of arachidonic acid in murine mast cells undergoing apoptosis
Authors: M A McAlexander
A N Fonteh
D Swan
T LaPorte
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: arachidonic acid metabolism; mast cells; apoptosis; cytokine depletion; unsaturated fatty acids
Affiliations: Department of Internal Medicine, Pulmonary and Critical Care Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27154, USA. 

Abstract:  The goal of this study was to examine arachidonic acid (AA) metabolism by murine bone marrow-derived mast cells (BMMC) during apoptosis induced by cytokine depletion. BMMC deprived of cytokines for 12-48 h displayed apoptotic characteristics. During apoptosis, levels of AA, but not other unsaturated fatty acids, correlated with the percentage of apoptotic cells. A decrease in both cytosolic phospholipase A(2) expression and activity indicated that cytosolic phospholipase A(2) did not account for AA mobilization during apoptosis. Free AA accumulation is also unlikely to be due to decreases in 5-lipoxygenase and/or cyclooxygenase activities, since BMMC undergoing apoptosis produced similar amounts of leukotriene B(4) and significantly greater amounts of PGD(2) than control cells. Arachidonoyl-CoA synthetase and CoA-dependent transferase activities responsible for incorporating AA into phospholipids were not altered during apoptosis. However, there was an increase in arachidonate in phosphatidylcholine (PC) and neutral lipids concomitant with a 40.7 +/- 8.1% decrease in arachidonate content in phosphatidylethanolamine (PE), suggesting a diminished capacity of mast cells to remodel arachidonate from PC to PE pools. Further evidence of a decrease in AA remodeling was shown by a significant decrease in microsomal CoA-independent transacylase activity. Levels of lyso-PC and lyso-PE were not altered in cells undergoing apoptosis, suggesting that the accumulation of lysophospholipids did not account for the decrease in CoA-independent transacylase activity or the induction of apoptosis. Together, these data suggest that the mole quantities of free AA closely correlated with apoptosis and that the accumulation of AA in BMMC during apoptosis was mediated by a decreased capacity of these cells to remodel AA from PC to PE. 

Retracted: No

PubPeer comments:
 Lots of dots are unexpected similar in different groups of Fig.1A. ![file] ,
Targeted gene correction in the mdx mouse using short DNA fragments: towards application with bone marrow-derived cells for autologous remodeling of dystrophic muscle
Authors: K Steeper
A F Quigley
E Byrne
P A Ioannou
R M Kapsa
A J Kornberg
J Vadolas
Journal: Gene Therapy (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: muscle; gene correction; bone marrow; dystrophic; cell therapy
Affiliations: Melbourne Neuromuscular Research Institute, Clinical Neurosciences, St Vincent's Hospital, Fitzroy Victoria, Australia.

Abstract:  In muscle, mutant genes can be targeted and corrected directly by intramuscular (i.m.) injection of corrective DNA, or by ex vivo delivery of DNA to myogenic cells, followed by cell transplantation. Short fragment homologous replacement (SFHR) has been used to repair the exon 23 nonsense transition at the Xp21.1 dys locus in cultured cells and also, directly in tibialis anterior from male mdx mice. Whilst mdx dys locus correction can be achieved in up to 20% of cells in culture, much lower efficiency is evident by i.m. injection. The major consideration for application of targeted gene correction to muscle is delivery throughout relevant tissues. Systemically injected bone marrow (BM)-derived cells from wt C57BL/10 ScSn mice are known to remodel mdx muscle when injected into the systemic route. Provided that non muscle-derived cell types most capable of muscle remodeling activity can be more specifically identified, isolated and expanded, cell therapy seems presently the most favorable vehicle by which to deliver gene correction throughout muscle tissues. Using wt bone marrow as a model, this study investigates systemic application of bone marrow-derived cells as potential vehicles to deliver corrected (ie wt) dys locus to dystrophic muscle. Intravenous (i.v.) and intraperitoneal (i.p.) injections of wt BM were given to lethally and sub-lethally irradiated mdx mice. Despite both i.v. and surviving i.p. groups containing wt dys loci in 100% and less than 1% of peripheral blood nuclei, respectively, both groups displayed equivalent levels of wt dys transcript in muscle RNA. These results suggest that the muscle remodeling activity observed in systemically injected BM cells is not likely to be found in the hemopoietic fraction. 

Retracted: No

PubPeer comments:
 This IEEE article [cited 84 times] according to Dimensions contains several [tortured phrases] that make some passages hard to parse: * **evacuation of noise** instead of the established _u2018noise reductionu2019_ * **proof of idea** instead of the established _u2018proof of conceptu2019_ * **vitality utilization** instead of the established _u2018energy useu2019_ * **brilliant (airport)** instead of the established _u2018smart (airport)u2019_ Can the authors explain why they departed from the established phrases? ![file] --- Free variables in RHS are not defined: ![file] --- Equation (9) reflects u2018Specificityu2019 and should be fixed accordingly: ![file] How come these incorrect wordings survived proofreading by the coauthors, editors, referees, copy editors, and typesetters? Found with the [_Problematic Paper Screener_] . ,
IL-1β suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury
Authors: Gadiparthi N Rao
Asrar B Malik
Shiqin Xiong
Ming Zhong
Wei Wu
Xiaopei Gao
Zhiming Ye
Anke Di
Saroj Nepal
Zhigang Hong
Jalees Rehman
Long Shuang Huang
Yoshikazu Tsukasaki
Dolly Mehta
Journal: Journal of Clinical Investigation (2020)
Discipline: CLINICAL MEDICINE
Keywords: Inflammation; Innate immunity; Vascular Biology; endothelial cells.
Affiliations: Department of Pharmacology and Regenerative Medicine and., Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, Illinois, USA., Department of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China., Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA.

Abstract:  Unchecked inflammation is a hallmark of inflammatory tissue injury in diseases such as acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS) and cecal ligation and puncture-induced (CLP-induced) polymicrobial sepsis decreased the expression of transcription factor cAMP response element binding (CREB) in lung endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin transcription and the formation of the normal restrictive endothelial adherens junctions. The inflammatory cytokine IL-1β reduced cAMP generation and CREB-mediated transcription of VE-cadherin. Furthermore, endothelial cell-specific deletion of CREB induced lung vascular injury whereas ectopic expression of CREB in the endothelium prevented the injury. We also observed that rolipram, which inhibits type 4 cyclic nucleotide phosphodiesterase-mediated (PDE4-mediated) hydrolysis of cAMP, prevented endotoxemia-induced lung vascular injury since it preserved CREB-mediated VE-cadherin expression. These data demonstrate the fundamental role of the endothelial cAMP-CREB axis in promoting lung vascular integrity and suppressing inflammatory injury. Therefore, strategies aimed at enhancing endothelial CREB-mediated VE-cadherin transcription are potentially useful in preventing sepsis-induced lung vascular injury in ARDS. 

Retracted: No

PubPeer comments:
 Figure 4. Four of the panels appear to overlap, as confirmed by ImageTwin. ![file] ,
Efficacy of co-administration of modified apple polysaccharide and probiotics in guar gum-Eudragit S100 based mesalamine mini tablets: A novel approach in treating ulcerative colitis
Authors: Souvik Mohanta
Jivan Jyoti
Sheetu Wadhwa
Ankit Kumar Yadav
Sananda Som
Rajesh Kumar
Narendra Kumar Pandey
Monica Gulati
Sachin Kumar Singh
Bimlesh Kumar
Kamal Dua
Journal: International Journal of Biological Macromolecules (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Mesalamine; Modified apple polysaccharide; Ulcerative colitis.
Affiliations: School of Pharmaceutical Sciences, Lovely Professional University, Phagwara 144411, Punjab, India., School of Pharmaceutical Sciences, Lovely Professional University, Phagwara 144411, Punjab, India.. Electronic address: ., Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Australia; School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia; Centre for Inflammation, Centenary Institute, Sydney, NSW 2050, Australia; Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute, Lot 1 Kookaburra Circuit, New Lambton Heights, Newcastle, NSW 2305, Australia.

Abstract:  Modified Apple Polysaccharide (MAP) has been reported to cure colorectal diseases by up-regulating apoptosis and down regulating metastasis. In the present study, mesalamine (MES) and MAP mini tablets have been prepared and co-administered with probiotics to provide site specific release of drug. Probiotics along with MAP, which acts as a prebiotic would replenish the colonic microflora that have been compromised due to colorectal pathology. MES mini tablets were prepared keeping guar gum in the core and coating them with Eudragit S100 and guar gum. The optimized batch was explored for its curative potential on acetic acid induced ulcerative colitis (UC) in rat model with and without administration of probiotic and MAP. The results revealed that the rats treated with the combination of MAP and MES mini tablets along with probiotics show maximum curative potential. It was also observed that MAP mini tablets show better curative potential as compared to probiotics. The results of disease activity index, macroscopic scoring, antioxidant studies, tumour alpha and histopathological examination suggested that the rats treated with combination of MES-MAP mini tablets and probiotics have maximum therapeutic effect followed by MES mini tablets alone, MAP mini tablets alone and probiotics. 

Retracted: No

PubPeer comments:
 ![file] , 
 In addition to #1, authors should really be careful to take correct pictures, i.e. perform white balance (all images) and set focus accurately (e.g. E1). The whole set is currently non-informative. ,
Effect of graphite oxide and exfoliated graphite oxide as a modifier for the voltametric determination of dopamine in presence of uric acid and folic acid
Authors: B E Kumara Swamy
S C Sharma
G K Jayaprakash
H Vidya
S A Hariprasad
Journal: Scientific Reports (2021)
Discipline: Multidisciplinary
Keywords: exfoliated graphite oxide; graphene oxide; electrocatalytic properties; dopamine; uric acid
Affiliations: Department of P. G. Studies and Research in Industrial Chemistry, Kuvempu University, Jnanasahyadri, Shankaraghatta, Shimoga, Karnataka, 577 451, India., Department of P. G. Studies and Research in Industrial Chemistry, Kuvempu University, Jnanasahyadri, Shankaraghatta, Shimoga, Karnataka, 577 451, India. ., National Assessment and Accreditation Council, Jain University, Bangalore, Karnataka, 560 069, India. ., School of Advanced Chemical Sciences, Shoolini University, Bajhol, Himachal Pradesh, 173229, India., Jain University, Bangalore, Karnataka, 560 069, India.

Abstract:  In the present work, exfoliated graphite oxide (E-GO) was prepared by sonicating graphite oxide (GO) (prepared by modified Hummer's and Offemam methods). Prepared GO and E-GO were characterized using infrared absorption spectroscopy, X-ray diffraction, and scanning electron microscopy. The electrocatalytic properties of GO and E-GO towards detection of dopamine (DA), uric acid (UA), and folic acid (FA) were investigated using cyclic voltammetry and differential pulse voltammetry. Our results revealed that E-GO has a slighter advantage over the GO as an electrode modifier for detection DA, UA, and FA, which might be ascribed to the good conductivity of E-GO when compared to the GO. 

Retracted: No

PubPeer comments:
 Figure 1 a Powder XRD patterns of GO and E-GO are identical, green pattern stretched along horizonal direction and drwan with thicker line. ![file] ,
Curcumin loaded poly (amidoamine) dendrimer-plamitic acid core-shell nanoparticles as anti-stress therapeutics
Authors: Suruchi Rai
Prashant Kesharwani
Ankur Shrivatava
Shalini Tripathi
Shraddha Gupta
Sima Singh
Pushpendra Kumar Tripathi
Ajay J Khopade
Journal: Drug Development and Industrial Pharmacy (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Curcumin; PAMAM dendrimer; antistress agent; drug delivery; palmitic acid nanoparticles.
Affiliations: Department of Pharmacy, RITM, Dr APJ Abdual Kalam Technical University, Lucknow, Uttar Pradesh, India., Discipline of Pharmaceutical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa., Sun Pharma Advanced Research Company Limited, Mumbai, India., Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.

Abstract:  Despite poor bioavailability of the drug and in vivo stability, curcumin has been reported for many pharmacological activities. Considering the potential of dendrimers as a drug delivery system, current research work is focused on the formulation and characterization of G4 PAMAM dendrimer-Palmitic acid core-shell nanoparticle-containing curcumin as antistress therapeutics to maximize the bioavailability of curcumin. Various formulations were prepared using different concentrations of palmitic acid and an optimized ratio of dendrimer and curcumin. All formulations were investigated for evaluation of physicochemical parameters, encapsulation efficiency, and in vitro release. Particle size, PDI, zeta-potential, and encapsulation efficiency of final formulation was found to be 257.9 ± 0.365 nm, 0.10 ± 0.004, 3.59 ± 0.167 mV, and 80.87%, respectively. In vitro release studies have shown that 53.62 ± 2.431% of the drug was released after 24 h. In vivo studies pharmacokinetic parameters, drug distribution, pharmacological, and toxicological were also estimated using swiss albino mice. The findings have shown the selected formulation is better than plain curcumin formulation. 

Retracted: No

PubPeer comments:
 Figure 4F image was cropped and duplicated in Figure 4D panel. Could authors clarify this duplication of the image? ![file] ,
Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells
Authors: Tomasz Stoklosa
Lori Rink
Artur Slupianek
Ilona Seferynska
Katarzyna Urbanska
Krzysztof Reiss
Margaret Nieborowska-Skorska
Tomasz Skorski
Journal: Blood (2007)
Discipline: CLINICAL MEDICINE
Keywords: Nbs1; ATM; DNA double-strand breaks; BCR/ABL; c-Myc
Affiliations: Department of Microbiology and Immunology, Temple University, Philadelphia, PA 19140, USA., Department of Microbiology and Immunology, Temple University, Philadelphia, PA;, Department of Immunology, Medical University of Warsaw, Poland;, Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Philadelphia, PA;, Department of Hematology, Institute of Hematology and Blood Transfusion, Warsaw, Poland

Abstract:  Nbs1, a member of the Mre11-RAD50-Nbs1 complex, is phosphorylated by ATM, the product of the ataxia-telangiectasia mutated gene and a member of the phosphatidylinositol 3-kinase-related family of serine-threonine kinases, in response to DNA double-strand breaks (DSBs) to regulate DNA damage checkpoints. Here we show that BCR/ABL stimulated Nbs1 expression by induction of c-Myc-dependent transactivation and protection from caspase-dependent degradation. BCR/ABL-related fusion tyrosine kinases (FTKs) such as TEL/JAK2, TEL/PDGFbetaR, TEL/ABL, TEL/TRKC, BCR/FGFR1, and NPM/ALK as well as interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), and stem cell factor (SCF) also stimulated Nbs1 expression. Enhanced ATM kinase-dependent phosphorylation of Nbs1 on serine 343 (S343) in response to genotoxic treatment was detected in leukemia cells expressing BCR/ABL and other FTKs in comparison to normal counterparts stimulated with IL-3, GM-CSF, and SCF. Expression of Nbs1-S343A mutant disrupted the intra-S-phase checkpoint, decreased homologous recombinational repair (HRR) activity, down-regulated XIAP expression, and sensitized BCR/ABL-positive cells to cytotoxic drugs. Interestingly, inhibition of Nbs1 phosphorylation by S343A mutant enhanced the antileukemia effect of the combination of imatinib and genotoxic agent. 

Retracted: No

PubPeer comments:
null, 
null, 
 Figure 3. Higher resolution. Much more similar than you would expect. https: imgur.com jaH0Rp1 , 
 Figure 2B. Much more similar than you would expect. https: imgur.com o86eX0k ,
miR-203 inhibits augmented proliferation and metastasis of hepatocellular carcinoma residual in the promoted regenerating liver
Authors: Ming-Qing Xu
Jian-Wei Tang
Xiao-Bo Chen
Peng-Sheng Yi
Lei Feng
Ming Zhang
Xiao-Bo Zheng
Liang-Liang Xu
Journal: Cancer science (2017)
Discipline: CLINICAL MEDICINE
Keywords: Hepatectomy; hepatocellular carcinoma; liver regeneration; miR-203 overexpression; proliferation and metastasis.
Affiliations: Department of Liver Surgery, West China Hospital, Sichuan University, Chengdu, China., Department of Hepatobiliary Surgery, The Affiliated Hospital of Kunming University of Science and Technology (the First People's Hospital of Yunnan Province), Kunming, China.

Abstract:  Liver resection is still the most commonly used therapeutic treatment for hepatocellular carcinoma (HCC), and liver regeneration promotes HCC growth in the regenerating liver. The high recurrence/metastasis of HCC is the main cause of death for HCC patients after liver resection. However, how the augmented growth and metastasis of residual HCC induced by the promoted liver regeneration following liver resection can be abolished remains unclear. In this study, a rat model with liver cirrhosis and diffused HCC was established by administration of diethylnitrosamine. Recombinant miR-203 adenovirus was administered to induce hepatic miR-203 overexpression and 30% partial hepatectomy (PH) followed. The effect of miR-203 on the proliferation, invasion and metastasis of the residual HCC in the remnant cirrhotic liver with promoted regeneration was investigated. We found that the basic spontaneous regeneration of the non-tumorous liver by 30% PH promoted proliferation, invasion and lung metastasis of the hepatic residual HCC. miR-203 overexpression further promoted the regeneration of the non-tumorous liver by upregulating Ki67 expression and enhancing IL-6/SOCS3/STAT3 pro-proliferative signals. Importantly, miR-203 overexpression markedly inhibited the proliferation, invasion and metastasis of hepatic residual HCC through suppressing expression of Ki67, CAPNS1 and lung metastasis. Moreover, it was found that miR-203 overexpression reversed the epithelial-mesenchymal transition induced by hepatectomy through targeting IL-1β, Snail1 and Twist1. In conclusion, our results suggested that miR-203 overexpression inhibited the augmented proliferation and lung metastasis of the residual HCC induced by the promoted liver regeneration following PH partly by regulating epithelial-mesenchymal transition. 

Retracted: No

PubPeer comments:
 Two images in figure 3a appear to overlap. *** Closeup showing approximate overlap ![file] *** Full figure showing location ![file] , 
 Also, the Tubulin bands in Figures 5 and 6 appear to be the same, but labeled differently. *** Closeup ![file] *** Full figure showing location ![file] ,
Translational Quality Control by Bacterial Threonyl-tRNA Synthetases
Authors: Mei-Qin Xue
Yong Wang
Ru-Juan Liu
En-Duo Wang
Zhi-Peng Fang
Yun Chen
Xiao-Long Zhou
Zhi-Rong Ruan
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: aminoacyl tRNA synthetase; protein synthesis; transfer RNA (tRNA); translation; translation control.
Affiliations: From the State Key Laboratory of Molecular Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China and., the School of Life Science and Technology, ShanghaiTech University, 200031 Shanghai, China., From the State Key Laboratory of Molecular Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031 Shanghai, China and the School of Life Science and Technology, ShanghaiTech University, 200031 Shanghai, China .

Abstract:  Translational fidelity mediated by aminoacyl-tRNA synthetases ensures the generation of the correct aminoacyl-tRNAs, which is critical for most species. Threonyl-tRNA synthetase (ThrRS) contains multiple domains, including an N2 editing domain. Of the ThrRS domains, N1 is the last to be assigned a function. Here, we found that ThrRSs from Mycoplasma species exhibit differences in their domain composition and editing active sites compared with the canonical ThrRSs. The Mycoplasma mobile ThrRS, the first example of a ThrRS naturally lacking the N1 domain, displays efficient post-transfer editing activity. In contrast, the Mycoplasma capricolum ThrRS, which harbors an N1 domain and a degenerate N2 domain, is editing-defective. Only editing-capable ThrRSs were able to support the growth of a yeast thrS deletion strain (ScΔthrS), thus suggesting that ScΔthrS is an excellent tool for studying the in vivo editing of introduced bacterial ThrRSs. On the basis of the presence or absence of an N1 domain, we further revealed the crucial importance of the only absolutely conserved residue within the N1 domain in regulating editing by mediating an N1-N2 domain interaction in Escherichia coli ThrRS. Our results reveal the translational quality control of various ThrRSs and the role of the N1 domain in translational fidelity. 

Retracted: No

PubPeer comments:
 Red box: the image background in Fig 3b is different. ![file] ,
Impaired nutrient signaling and body weight control in a Na+ neutral amino acid cotransporter (Slc6a19)-deficient mouse
Authors: Nadine Tietze
Jessica M Vanslambrouck
Angelika Bröer
Torsten Juelich
Jeff Holst
Peter S Solomon
Charles G Bailey
John E J Rasko
Stefan Bröer
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Amino acid uptake; intestine; kidney; transporters; neutral amino acid
Affiliations: Research School of Biology, Australian National University, Canberra, Australian Capital Territory 0200, Australia. 

Abstract:  Amino acid uptake in the intestine and kidney is mediated by a variety of amino acid transporters. To understand the role of epithelial neutral amino acid uptake in whole body homeostasis, we analyzed mice lacking the apical broad-spectrum neutral (0) amino acid transporter B(0)AT1 (Slc6a19). A general neutral aminoaciduria was observed similar to human Hartnup disorder which is caused by mutations in SLC6A19. Na(+)-dependent uptake of neutral amino acids into the intestine and renal brush-border membrane vesicles was abolished. No compensatory increase of peptide transport or other neutral amino acid transporters was detected. Mice lacking B(0)AT1 showed a reduced body weight. When adapted to a standard 20% protein diet, B(0)AT1-deficient mice lost body weight rapidly on diets containing 6 or 40% protein. Secretion of insulin in response to food ingestion after fasting was blunted. In the intestine, amino acid signaling to the mammalian target of rapamycin (mTOR) pathway was reduced, whereas the GCN2/ATF4 stress response pathway was activated, indicating amino acid deprivation in epithelial cells. The results demonstrate that epithelial amino acid uptake is essential for optimal growth and body weight regulation. 

Retracted: No

PubPeer comments:
 ![file] ,
TGF-β1 mediates epithelial to mesenchymal transition via the TGF-β/Smad pathway in squamous cell carcinoma of the head and neck
Authors: Changyun Yu
Ting Xu
Xin Zhang
Yaozhang Dai
Yongquan Tian
Jinjie Sun
Gengming Cai
Donghai Huang
Yong Liu
Journal: Oncology Reports (2011)
Discipline: CLINICAL MEDICINE
Keywords: metastasis; squamous cell carcinoma; head and neck; epithelial to mesenchymal transition; EMT
Affiliations: Department of Otolaryngology, Xiangya Hospital, Central South University, Xiangya Road 87, Changsha 410008, Hunan, PR China.

Abstract:  Development of metastasis is a major cause of death for squamous cell carcinoma of the head and neck (SCCHN) patients. Epithelial to mesenchymal transition (EMT) is now regarded as a correlate of tumor metastasis. Given that transforming growth factor-β1 (TGF-β1) is an important inducer of EMT, we examined the effects of TGF-β1 on the human SCCHN cell line Tu686. We found that TGF-β1 mediated cell morphological changes. Phase-contrast microscopy revealed a loss of the adherent phenotype with cellular elongation, decrease in cell-to-cell contact, and the induction of a fibroblast-like state. Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated that TGF-β1 could induce down-regulation of the epithelial marker E-cadherin and up-regulation of the mesenchymal marker vimentin in Tu686 cells in a concentration- and time-dependent manner. Wound- healing and transwell invasion assay indicated that TGF-β1 promoted Tu686 cell migration and invasion dramatically. In addition, these changes were mediated via canonical TGF-β/Smad signaling with concomitant up-regulation of phosphorylated Smad2. Smad2 RNAi abrogated both expression and functional effects of TGF-β1 on Tu686 cells. In conclusion, the present study demonstrates that TGF-β1 could induce EMT in the SCCHN cell line via the TGF-β/Smad signaling pathway. More importantly, a cell model for EMT was established, which is valuable for future studies on the metastasis of SCCHN. 

Retracted: No

PubPeer comments:
 Figures 2C and 4D appear to include an area of overlap. *** ![file] ,
Single atom tungsten doped ultrathin α-Ni(OH)2 for enhanced electrocatalytic water oxidation
Authors: Lingqiao Kong
Shuit-Tong Lee
Junqing Yan
Yujin Ji
Jing Zhang
Tianyi Ma
Pengfei An
Jai White
Shengzhong Liu
Youyong Li
Journal: Nature Communications (2019)
Discipline: Multidisciplinary
Keywords: Electrocatalytic water oxidation; W6+ doping; Ni(OH)2 nanosheet; oxygen evolution reaction (OER); overpotential
Affiliations: Key Laboratory of Applied Surface and Colloid Chemistry, Ministry of Education; Shaanxi Engineering Lab for Advanced Energy Technology, School of Materials Science and Engineering, Shaanxi Normal University, Xi'an, 710119, People's Republic of China., Institute of Functional Nano & Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials & Devices, Soochow University, Suzhou, Jiangsu, 215123, People's Republic of China., Discipline of Chemistry, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, 2308, Australia., Institute of Functional Nano & Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials & Devices, Soochow University, Suzhou, Jiangsu, 215123, People's Republic of China. ., Beijing Synchrotron Radiation Facility, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, 100049, People's Republic of China., Key Laboratory of Applied Surface and Colloid Chemistry, Ministry of Education; Shaanxi Engineering Lab for Advanced Energy Technology, School of Materials Science and Engineering, Shaanxi Normal University, Xi'an, 710119, People's Republic of China. ., Discipline of Chemistry, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, 2308, Australia. .

Abstract:  Electrocatalytic water oxidation is a rate-determining step in the water splitting reaction. Here, we report one single atom W6+ doped Ni(OH)2 nanosheet sample (w-Ni(OH)2) with an outstanding oxygen evolution reaction (OER) performance that is, in a 1 M KOH medium, an overpotential of 237 mV is obtained reaching a current density of 10 mA/cm2. Moreover, at high current density of 80 mA/cm2, the overpotential value is 267 mV. The corresponding Tafel slope is measured to be 33 mV/dec. The d0 W6+ atom with a low spin-state has more outermost vacant orbitals, resulting in more water and OH- groups being adsorbed on the exposed W sites of the Ni(OH)2 nanosheet. Density functional theory (DFT) calculations confirm that the O radical and O-O coupling are both generated at the same site of W6+. This work demonstrates that W6+ doping can promote the electrocatalytic water oxidation activity of Ni(OH)2 with the highest performance. 

Retracted: No

PubPeer comments:
 1. In supplementary Figure 4, the noise background is unexpected similar by multiplying a constant value, which is impossible generated by instrument. Also some vibration bumps are very weird. ![file] 2. Similar noise patterns with certain scale are also observed for supplementary Figure 20. ![file] ,
Upregulation of miR-132 attenuates osteoblast differentiation of UC-MSCs
Authors: J-H Ge
Z-L Xue
Y-L Meng
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Wnt/β-catenin signaling pathway; miR-132; Osterix; OB differentiation; umbilical cord mesenchymal stem cells (UC-MSCs)
Affiliations: Shanghai Jiading Nanxiang Hospital, Shanghai, China. .

Abstract:  Objective: Wnt/β-catenin signaling pathway plays a role in upregulating expression of osteoblast (OB) specific transcriptional factor Osterix and promoting OB differentiation. It was shown that the elevation of the miR-132 level was associated with sclerotizing inhibition. Bioinformatics analysis revealed the complementary binding site between miR-132 and 3'-UTR of β-catenin. This study investigated the influence of miR-214 in regulating β-catenin expression and differentiation of umbilical cord mesenchymal stem cells (UC-MSCs) into OB. Materials and methods: UC-MSCs were induced to differentiate to OB. The expressions of miR-132, β-catenin, Osterix, and ALP, together with ALP activity were detected on day 0, 5, 10, and 15. The regulatory relationship between miR-132 and β-catenin was confirmed by dual luciferase reporter gene assay. UC-MSCs were divided into five groups, including agomir-control, miR-132 agomir, pGPH1-NC, pGPH1-β-catenin, and miR-132 agomir + pGPH1-β-catenin groups. β-catenin, Osterix, and ALP expressions, together with ALP activity were tested after induction for 15 days. Results: MiR-132 was downregulated, while β-catenin Osterix and ALP expressions, together with ALP activity were enhanced in the process of UC-MSCs differentiating into OBs. MiR-132 agomir and/or pGPH1-β-catenin transfection significantly reduced β-catenin expression, downregulated Wnt/β-catenin signaling pathway activity, declined Osterix level, weakened ALP expression and activity, and attenuated OB differentiation of UC-MSCs. Conclusions: The level of β-catenin was enhanced, while the miR-132 level was decreased in the process of UC-MSCs differentiating into OBs. Upregulation of miR-132 inhibited the differentiation of UC-MSCs through suppressing β-catenin expression, attenuating Wnt/β-catenin signaling pathway activity, and downregulating Osterix level. 

Retracted: No

PubPeer comments:
 This paper has features suggestive of [what has elsewhere been labeled as  Papermill #2 ] , characterised by stylised geometrical WBs that are reduced to sharp-edged black ovals on a featureless grey background, reminiscent of a Miro painting: ![file] ![file] ![file] Other examples are listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit?usp=sharing ,