PReD-Bench/PRed-Bench huggingface dataset:
ASC-J9 ameliorates spinal and bulbar muscular atrophy phenotype via degradation of androgen receptor
Authors: Lu-Min Chen
Hiroshi Miyamoto
Chawnshang Chang
Cheng-Chia Wu
Diane E Merry
Gen Sobue
Yu-Jia Chang
I-Chen Yu
Shuyuan Yeh
Zhiming Yang
Shu-Shi Chang
Journal: Nature Medicine (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Motor neuron degeneration; androgen receptor; polyglutamine tract; spinal and bulbar muscular atrophy; Kennedy disease
Affiliations: George Whipple Lab for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, and The Cancer Center, University of Rochester Medical Center, Rochester, New York 14642, USA.

Abstract:  Motor neuron degeneration resulting from the aggregation of the androgen receptor with an expanded polyglutamine tract (AR-polyQ) has been linked to the development of spinal and bulbar muscular atrophy (SBMA or Kennedy disease). Here we report that adding 5-hydroxy-1,7-bis(3,4-dimethoxyphenyl)-1,4,6-heptatrien-3-one (ASC-J9) disrupts the interaction between AR and its coregulators, and also increases cell survival by decreasing AR-polyQ nuclear aggregation and increasing AR-polyQ degradation in cultured cells. Intraperitoneal injection of ASC-J9 into AR-polyQ transgenic SBMA mice markedly improved disease symptoms, as seen by a reduction in muscular atrophy. Notably, unlike previous approaches in which surgical or chemical castration was used to reduce SBMA symptoms, ASC-J9 treatment ameliorated SBMA symptoms by decreasing AR-97Q aggregation and increasing VEGF164 expression with little change of serum testosterone. Moreover, mice treated with ASC-J9 retained normal sexual function and fertility. Collectively, our results point to a better therapeutic and preventative approach to treating SBMA, by disrupting the interaction between AR and AR coregulators. 

Retracted: No

PubPeer comments:
 Figure 1D, lower panels. * Orange boxes: The left ERa panel looks similar to the right AR panel * Green boxes: The left AR panel looks similar to the right ERa panel.  , 
 Figure 6A. * Aqua boxes: The left and right IB:CBP panels look very similar. Could the authors clarify if these two panels represent a different cell line or some other different experiment? The labeling is not clear, but they are presented as two separate panels. * Red boxes: Lanes 1-3 in the left IB:AR panels look very similar to lanes 3-5 in the bottom left Actin panel in Figure 1C. Note the slanted shape of the right-most lane.  ,
LNC00673 suppresses proliferation and metastasis of pancreatic cancer via target miR-504/ HNF1A
Authors: Yi Gong
Wei Liu
Jun-Jie Shu
Ping Bie
Lei-da Zhang
Hai-Su Dai
Journal: Journal of Cancer (2020)
Discipline: CLINICAL MEDICINE
Keywords: LINC00673; Metastasis; MiR-504/HNF1A; Pancreatic Cancer; Proliferation.
Affiliations: Department of Hepatobiliary Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, China.

Abstract:  Pancreatic cancer is a highly invasive malignant tumor of the digestive system. To explore the mechanism of pancreatic cancer development, development, invasion and metastasis, in this study we focused on long non-coding RNA (LncRNA), which has been reported to be involved in tumorigenesis. We identified a LINC00673, which is highly correlated with the pancreatic cancer risk. LINC00673 Overexpression is associated with good survival in pancreatic cancer patients, Effects of LINC00673 on pancreatic cancer cell apoptosis, viability, migration. LINC00673 negatively correlated with miR-504 and MiR-504 overexpression promoted cancer progression in Pancreatic cancer. MiR-504 negatively correlated with HNF1A, which was highly expressed Pancreatic cancer. HNF1A inhibited cell progression in pancreatic cancer cells. LINC00673 overexpression inhibited caner progression in nude mice. Taken together, LINC00673 can through suppress miR-504/ HNF1A regulating invasion and migration in pancreatic cancer. Also, we identified miR-504 as a target of LINC00673 in pancreatic cancer and LINC00673 can be used as a novel therapeutic target for the pancreatic cancer. 

Retracted: No

PubPeer comments:
 The mechanism that Fgl2 interacts with TLR4 is absolutely made. We previously dissect the involvement of Fgl2 in inflammatory signaling in Dr. Qin Ning lab but these data idea was copied by Dr. Xiaojing Wang. I think Dr. Wang should go back to April 2018 when she ask our manuscript and figures of  Fibrinogen-like protein 2 deficiency inhibits virus-induced fulminant hepatitis through abrogating inflammatory macrophage activation for reference and eventually she published the same data of the mechanism of Fgl2 in inflammatory signalling. Importantly, in our manuscript we hypothesized that the mechanism underlying how Fgl2 regulates inflammation may be mediated by interacting with TLR4 thereby enhancing inflammation signaling. However, we denied such hypothesis because my MS data from high-affinity purification with Flag-tagged Fgl2 (Flag at C terminal) in both THP1 and 293T cells did not include TLR4. So, such data is not trustworthy. Another point is that all mice were raised in non-pathogen free conditions in making the whole paper not believable. ,
Glutathione is recruited into the nucleus in early phases of cell proliferation
Authors: Juan Sastre
Jelena Markovic
Jos√© Vi√±a
Federico V Pallard√≥
Angel Ortega
Consuelo Borr√°s
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: nuclear glutathione distribution; cell cycle progression; confocal microscopy; flow cytometry; protein expression
Affiliations: Department of Physiology, Faculty of Medicine, University of Valencia, Avenida Blasco Ib√°√±ez 17, 46010 Valencia, Spain.

Abstract:  We have studied the possible correlation between nuclear glutathione distribution and the progression of the cell cycle. The former was studied by confocal microscopy using 5-chloromethyl fluorescein diacetate and the latter by flow cytometry and protein expression of Id2 and p107. In proliferating cells, when 41% of them were in the S+G(2)/M phase of the cell cycle GSH was located mainly in the nucleus. When cells reached confluence (G(0)/G(1)) GSH was localized in the cytoplasm with a perinuclear distribution. The nucleus/cytoplasm fluorescence ratio for GSH reached a maximal mean value of 4.2 +/- 0.8 at 6 h after cell plating. A ratio higher than 2 was maintained during exponential cell growth. In the G(0)/G(1) phase of the cell cycle, the nucleus/cytoplasm GSH ratio decreased to values close to 1. We report here that cells concentrate GSH in the nucleus in the early phases of cell growth, when most of the cells are in an active division phase, and that GSH redistributes uniformly between the nucleus and the cytoplasm when cells reach confluence. 

Retracted: No

PubPeer comments:
 Figure 5. Much more similar than you would expect. https: imgur.com OKLN08B ,
<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>
Authors: Zhenling Zhang
Fenghua Lv
Changlei Guo
Guoan Zhao
Aoyang Si
Liangping Zhao
Peiyong Zhang
Junbiao Zhang
Journal: Drug Design Development and Therapy (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Ginkgolide B; apoptosis PI3K/AKT/mTOR pathway; endoplasmic reticulum stress; myocardial injury.
Affiliations: Department of Cardiology, The First Affiliated Hospital Xinxiang Medical University, Weihui 452100, Henan, China, .

Abstract:  Purpose: Ginkgolide B (GB) is a terpene lactone component found in Ginkgo biloba, which has a protective role on ischemia reperfusion (I/R) injury. This study was aimed at exploring the protective mechanism of GB on the myocardial I/R. Patients and methods: Myocardial I/R model was established on Sprague Dawley rats. The levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin were determined by a 200FR NEO automatic biochemical analyzer. Histological examination was performed through HE and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The expression levels of p-PERK, p-IRE1Œ±, ATF6, p-AKT, and mTOR were detected by Western blot. Results: The results exhibited that GB treatment suppressed the high levels of cardiac troponin I, cardiac troponin T, lactic dehydrogenase, and myoglobin and ameliorated the damaged and irregularly arranged myocardial cells induced by I/R injury significantly, indicating that GB could ameliorate myocardial I/R injury. Moreover, the high expression levels of endoplasmic reticulum (ER) stress key proteins caused by I/R injury were suppressed significantly by GB treatment, including p-PERK, p-IRE1Œ±, and ATF6. GB treatment also decreased the number of apoptotic cells compared with I/R group. In addition, activation of ER stress by Tunicamycin treatment could counteract the protective effects of GB on I/R injury, suggesting that GB ameliorated myocardial I/R injury through inhibition of ER stress-induced apoptosis. Finally, the decreased p-AKT and p-mTOR expressions caused by I/R injury were upregulated by GB and inhibition of PI3K/AKT/mTOR pathway by LY294002 abolished the protective effects of GB on I/R injury, indicating that GB activated PI3K/AKT/mTOR pathway during I/R injury. Conclusion: GB protected against myocardial I/R injury through inhibiting ER stress-induced apoptosis via PI3K/AKT/mTOR signaling pathway. 

Retracted: Yes

PubPeer comments:
 Figure 6. Much more similar than expected.  ,
ABCA8 is regulated by miR-374b-5p and inhibits proliferation and metastasis of hepatocellular carcinoma through the ERK/ZEB1 pathway
Authors: Jizhou Wang
Lianxin Liu
Yifeng Cui
Yan Wang
Hongrui Guo
Shugeng Zhang
Shangha Pan
Fanzheng Meng
Yunzheng Zhao
Yao Liu
Ruipeng Song
Xirui Liu
Bo Zhang
Jiabei Wang
Congyi Zhang
Shuhang Liang
Dalong Yin
Jihua Han
Dehai Wu
Zhaoyang Lu
Journal: Journal of Experimental & Clinical Cancer Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: ATP binding cassette subfamily a member 8; Epithelial to mesenchymal transition; Hepatocellular carcinoma; Therapeutic target.
Affiliations: Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China., Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Harbin, Heilongjiang, China., Department of Hepatobiliary Surgery, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China., Department of Colorectal Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China., Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. ., Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Harbin, Heilongjiang, China. ., Department of Hepatobiliary Surgery, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China. .

Abstract:  Background: ATP binding cassette subfamily A member 8 (ABCA8) belongs to the ATP binding cassette (ABC) transporter superfamily. ABCA8 is a transmembrane transporter responsible for the transport of organics, such as cholesterol, and drug efflux. Some members of the ABC subfamily, such as ABCA1, may inhibit cancer development. However, the mechanism of ABCA8 in the process of cancer activation is still ambiguous. Methods: The expression of ABCA8 in human hepatocellular carcinoma (HCC) tissues and cell lines was examined using qPCR, immunoblotting, and immunohistochemical staining. The effects of ABCA8 on the proliferation and metastasis of HCC were examined using in vitro and in vivo functional tests. A luciferase reporter assay was performed to explore the binding between microRNA-374b-5p (miR-374b-5p) and the ABCA8 3'-untranslated region (UTR). Results: ABCA8 was frequently down-regulated in HCC and this down-regulation was negatively correlated with prognosis. The overexpression of ABCA8 inhibited growth and metastasis in HCC, whereas the knockdown of ABCA8 exerted the antithetical effects both in vivo and in vitro. ABCA8 was down-regulated by miR-374b-5p; this down-regulation can induce epithelial transformation to mesenchyme via the ERK/ZEB1 signaling pathway and promote HCC progression. Conclusion: We exposed the prognostic value of ABCA8 in HCC, and illuminated a novel pathway in ABCA8-regulated inhibition of HCC tumorigenesis and metastasis. These findings may lead to a new targeted therapy for HCC through the regulation of ABCA8, and miR-374b-5p. 

Retracted: No

PubPeer comments:
  So many overlaps in this figure. ,
Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice
Authors: Hemachandra Mahaseth
Gregory M Vercellotti
Thomas E Welch
Leo E Otterbein
Robert P Hebbel
John D Belcher
Journal: Journal of Clinical Investigation (2006)
Discipline: CLINICAL MEDICINE
Keywords: Transgenic sickle mice; betaS hemoglobin; vascular endothelium; NF-kappaB; adhesion molecules
Affiliations: Division of Hematology, Oncology, and Transplantation, Department of Medicine and Vascular Biology Center, University of Minnesota, Minneapolis, Minnesota 55455, USA. 

Abstract:  Transgenic sickle mice expressing betaS hemoglobin have activated vascular endothelium that exhibits enhanced expression of NF-kappaB and adhesion molecules that promote vascular stasis in sickle, but not in normal, mice in response to hypoxia/reoxygenation. Sickle mice hemolyze rbcs in vivo as demonstrated by increased reticulocyte counts, plasma hemoglobin and bilirubin, and reduced plasma haptoglobin. The heme content is elevated in sickle organs, which promotes vascular inflammation and heme oxygenase-1 expression. Treatment of sickle mice with hemin further increases heme oxygenase-1 expression and inhibits hypoxia/reoxygenation-induced stasis, leukocyte-endothelium interactions, and NF-kappaB, VCAM-1, and ICAM-1 expression. Heme oxygenase inhibition by tin protoporphyrin exacerbates stasis in sickle mice. Furthermore, treatment of sickle mice with the heme oxygenase enzymatic product carbon monoxide or biliverdin inhibits stasis and NF-kappaB, VCAM-1, and ICAM-1 expression. Local administration of heme oxygenase-1 adenovirus to subcutaneous skin increases heme oxygenase-1 and inhibits hypoxia/reoxygenation-induced stasis in the skin of sickle mice. Heme oxygenase-1 plays a vital role in the inhibition of vaso-occlusion in transgenic sickle mice. 

Retracted: No

PubPeer comments:
 Fig. 6A u2013 more similar than expected could authors check please?  , 
 #1 Figure 6A continued. Much more similar than expected. https: imgur.com bjEeYQi , 
 I will look into this further! ,
Endothelin-1 induces expression of matrix-associated genes in lung fibroblasts through MEK/ERK
Authors: Andrew Leask
Roland M du Bois
Alan Holmes
Christopher P Denton
Sarah L Howat
David J Abraham
Jeremy D Pearson
Shi-wen Xu
Elisabetta A Renzoni
Carol M Black
Michael R Dashwood
George Bou-Gharios
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Endothelins; vasoconstriction; ET-1; lung fibroblasts; matrix genes
Affiliations: Centre for Rheumatology, Department of Medicine, Royal Free and University College London, United Kingdom.

Abstract:  The endothelins are a family of endothelium-derived peptides that possess a variety of biological activities, including potent vasoconstriction. Endothelin-1 (ET-1) is up-regulated during tissue repair and pulmonary fibrosis. Here, we use genome-wide expression array analysis to show that the addition of ET-1 (100 nm, 4 h) to normal lung fibroblasts directly induces expression of matrix and matrix-associated genes, including the profibrotic protein CCN2 (connective tissue growth factor, or CTGF). ET-1 induces the MEK/ERK MAP kinase pathway in fibroblasts. Blockade of the MEK/ERK kinase pathway with U0126 abrogates the ability of ET-1 to induce expression of matrix and matrix-associated mRNAs and the CCN2 protein. The CCN2 promoter possesses an ET-1 response element, which maps to the previously identified basal control element-1 (BCE-1) site. Our results suggest that ET-1 induces a program of matrix synthesis in lung fibroblasts and that ET-1 may play a key role in connective tissue deposition during wound repair and in pulmonary fibrosis. 

Retracted: No

PubPeer comments:
  , 
 Much more similar than you would expect. https: imgur.com r9oaYz9 ,
Parity and the association with diabetes in older women
Authors: Janet M Catov
Kenneth J Mukamal
Lewis H Kuller
Mercedes R Carnethon
Angela G Fowler-Brown
Aruna Kamineni
Ian H de Boer
David S Siscovick
Journal: Diabetes Care (2010)
Discipline: CLINICAL MEDICINE
Keywords: Parity; Diabetes; Glucose homeostasis; Older women; Grand multiparity
Affiliations: Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. 

Abstract:  Objective: To examine the relationship of parity with diabetes and markers of glucose homeostasis in older women. Research design and methods: We used data from the female participants in the Cardiovascular Health Study, a longitudinal cohort of adults aged &gt;or=65 years. These data included an assessment of parity (baseline) and fasting serum levels of glucose, insulin, and medication use (baseline and follow-up). We estimated both the cross-sectional relationship of parity with baseline diabetes and the relationship of parity with incident diabetes. Results: In unadjusted analyses, women with grand multiparity (&gt;or=5 live births) had a higher prevalence of diabetes at baseline compared with those with fewer births and with nulliparous women (25 vs. 12 vs. 15%; P &lt; 0.001). In regression models controlling for age and race, grand multiparity was associated with increased prevalence of diabetes (prevalence ratio 1.57 [95% CI 1.20-2.06]); with addition of demographic and clinical factors to the model, the association was attenuated (1.33 [1.00-1.77]). In final models that included body anthropometrics, the association was no longer significant (1.21 [0.86-1.49]). In those without diabetes at baseline, parity was not associated with incident diabetes or with fasting glucose; however, there was a modest association of parity with fasting insulin and homeostasis assessment model of insulin resistance. Conclusions: Grand multiparity is associated with diabetes in elderly women in cross-sectional analyses. This relationship seems to be confounded and/or mediated by variation in body weight and sociodemographic factors by parity status. In older nondiabetic women, higher parity does not pose an ongoing risk of developing diabetes. 

Retracted: No

PubPeer comments:
 Table 1 looks like it has some errors. Specifically, the counts and percentages for the black race groups don t seem to add up. It says there are 118 of 500 nulliparous women and that this represents 20.8% of the sample. However, 118 500*100=23.6%. The remainder of the percentages for black race seem to also be off as do some of the other values in the table. Am I misunderstanding what is intended in this table or is it wrong? ,
Aflatoxin B1 induced upregulation of protein arginine methyltransferase 5 in human cell lines
Authors: Md Sajid Ghufran
Santosh R Kanade
Krishna Ghosh
Journal: Toxicon (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Aflatoxin; Arginine methylation; Aspergillus flavus; PRMT5; SDMA.
Affiliations: Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasargod, Kerala, 671314, India., Department of Biochemistry and Molecular Biology, Central University of Kerala, Kasargod, Kerala, 671314, India. Electronic address: .

Abstract:  The exposure of naturally occurring mycotoxins affects human health and play a vital role in cancer initiation and progression. Aflatoxin B1 is a difuranocoumarin mycotoxin, classified as a group I carcinogen. The present study was conducted to assess the effect of aflatoxin B1 on epigenetic regulatory proteins. The protein arginine methyltransferase 5 expression was induced upon aflatoxin B1 treatment in a dose and time dependent manner. Further global arginine methylation was also increased in the same manner. This is the first report showing the induction of epigenetic regulatory protein, protein arginine methyltransferase 5 upon aflatoxin B1 treatment. Further study is required to establish the detailed pathway of PRMT5 induction. 

Retracted: No

PubPeer comments:
 In Figure 2E, part of a Western immunoblot has been duplicated, modified (including stretched vertically) and presented as something else.  ,
Bone marrow mononuclear cells exert long-term neuroprotection in a rat model of ischemic stroke by promoting arteriogenesis and angiogenesis
Authors: Chao Jiang
Jianping Wang
Lie Yu
Jian Wang
Ming Chen
Chunying Ou
Journal: Brain Behavior and Immunity (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Angiogenesis; Arteriogenesis; BMMNCs; Cerebral ischemia; Functional recovery
Affiliations: Department of Neurology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 Henan, China. Electronic address: .

Abstract:  Transplanted bone marrow-derived mononuclear cells (BMMNCs) can promote arteriogenesis and angiogenesis by incorporating into vascular walls and differentiating into smooth muscle cells (SMCs) and endothelial cells (ECs). Here, we explored whether BMMNCs can enhance arteriogenesis and angiogenesis and promote long-term functional recovery in a rat model of permanent middle cerebral artery occlusion (pMCAO). Sprague-Dawley rats were injected with vehicle or 1√ó10(7) BMMNCs labeled with BrdU via femoral vein 24 h after induction of pMCAO. Functional deficits were assessed weekly through day 42 after pMCAO, and infarct volume was assessed on day 7. We visualized the angioarchitecture by latex perfusion on days 14 and 42. BMMNC transplantation significantly reduced infarct volume and neurologic functional deficits compared with untreated or vehicle-treated ischemic groups. In BMMNC-treated rats, BrdU-positive cells were widely distributed in the infarct boundary zone, were incorporated into vessel walls, and enhanced the growth of leptomeningeal anastomoses, the circle of Willis, and basilar arteries. BMMNCs were shown to differentiate into SMCs and ECs from day 14 after stroke and preserved vascular repair function for at least 6 weeks. Our data indicate that BMMNCs can significantly enhance arteriogenesis and angiogenesis, reduce infarct volume, and promote long-term functional recovery after pMCAO in rats. 

Retracted: No

PubPeer comments:
 Editor [Expression of Concern] issued recently. [Another paper of the same group] also has an EOC. The editors of Brain Behaviour and Immunity issue this expression of concern regarding the above papers for the following reasons: u2022 there appears to be duplication of images presenting the immunocytochemistry data, as evident in the similarity between various panels in the figures (for example, 5q and 7d; or 6k and 7h); u2022 we have received no reply to our repeated requests for clarifications from the senior author or other authors involved in the publications. At this stage it is impossible to determine if these are genuine mistakes or evidence of scientific misconduct, but the duplication of figure raises concerns on the accuracy of the conclusions reached by the paper. ,
CD38 knockout suppresses tumorigenesis in mice and clonogenic growth of human lung cancer cells
Authors: David S Schrump
Joel Moss
Maria J Merino
Frances E Lund
Jiro Kato
Julie A Hong
Xiangning Bu
Journal: Carcinogenesis (2018)
Discipline: CLINICAL MEDICINE
Keywords: CD38; tumor formation; cancer therapy; ADP-ribose; NAD glycohydrolase
Affiliations: Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA., Thoracic Epigenetics Section, Thoracic and GI Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA., Translational Surgical Pathology, National Cancer Institute, Bethesda, MD, USA., Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.

Abstract:  The ectodomain of the plasma membrane ectoenzyme CD38 functions as both an NAD glycohydrolase and an ADP-ribosyl cyclase by catalyzing, respectively, the conversion of NAD to nicotinamide and ADP-ribose or cyclic ADP-ribose. CD38 is attracting particular attention in cancer therapy. An anti-CD38 monoclonal antibody (daratumumab) was approved for treatment of patients with multiple myeloma. However, the role of CD38 in non-hematological malignancies has not been explored. Previously, we reported that ADP-ribose-acceptor hydrolase (ARH)-1 deficiency in mice was associated with tumor development. In the present study, we found that in wild-type and ARH1-deficient mice deletion of the CD38 gene reduced tumor formation. Significant reductions in tumor number were observed in lymphomas, adenocarcinomas and hemangio/histolytic sarcomas. Consistent with a role for CD38 in tumorigenesis, CRISPR/Cas9-based knockout of CD38 in A549 human adenocarcinoma cells inhibited anchorage-independent cell growth, cell invasion and xenograft growth in nude mice. CD38 mRNA and protein expression were evaluated in human lung cancer cell lines and in human lung cancer specimens. CD38 overexpression in tumor cells was identified in 11 of 27 patient samples. In addition, some human lung cancer cell lines had dramatically higher CD38 mRNA and protein expression than normal cells. Consistent with these observations, search of the Oncomine database showed that some human lung adenocarcinomas had higher CD38 mRNA levels compared to normal lung tissues. In total, our data are consistent with the conclusion that CD38 plays a role in murine and human lung tumorigenesis and that anti-CD38 treatment may have therapeutic potential in lung cancer. 

Retracted: No

PubPeer comments:
 Dear authors, Could you please check Fig.5 in your publication? The tumor growth curves in A (female) and B (male) seem to be 100% identical.  ,
Halloysite Nanotube-Ferrihydrite Incorporated Polyethersulfone Mixed Matrix Membrane: Effect of Nanocomposite Loading on the Antifouling Performance
Authors: Norhaniza Yusof
Farhana Aziz
Ahmad Fauzi Ismail
Normi Izati Mat Nawi
Norazanita Shamsuddin
Syarifah Nazirah Wan Ikhsan
Muhammad Roil Bilad
Journal: Polymers (2021)
Discipline: CHEMISTRY
Keywords: halloysite nanotube; hydrous ferric oxide; loading effect; mixed matrix membrane; nanocomposite.
Affiliations: Advanced Membrane Technology Research Centre (AMTEC), N29A, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia., School of Chemical and Energy Engineering, Faculty of Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia., Department of Chemical Engineering, Universiti Teknologi Petronas (UTP), Bandar Seri Iskandar 32610, Malaysia., Faculty of Integrated Technologies, Universiti Brunei Darussalam, Bandar Seri Begawan BE1410, Brunei.

Abstract:  Membrane filtration is an attractive process in water and wastewater treatment, but largely restricted by membrane fouling. In this study, the membrane fouling issue is addressed by developing polyethersulfone (PES)-based mixed matrix membranes (MMMs) with the incorporation of hydrophilic nanoparticles as an additive. Ultrafiltration MMMs were successfully fabricated by incorporating different loadings of halloysite nanotube-ferrihydrates (HNT-HFO) into a polyethersulfone (PES) matrix and their performance was evaluated for the separation of bovine serum albumin (BSA) solution and oil/water emulsion. The results show that wettability is endowed to the membrane by introducing the additive aided by the presence of abundant -OH groups from the HFO. The loading of additive also leads to more heterogeneous surface morphology and higher pure water fluxes (516.33-640.82 L/m2h) more than twice that of the pristine membrane as reference (34.69 L/m2h) without affecting the rejection. The MMMs also provide much enhanced antifouling properties. The filtration results indicate that the flux recovery ratio of the modified membrane reached 100% by washing with only distilled water and a total flux recovery ratio of &gt;98% ¬± 0.0471 for HNT-HFO-loaded membranes in comparison with 59% ¬± 0.0169 for pristine PES membrane. 

Retracted: No

PubPeer comments:
 It appears that at least one image in Figure 2 is misplaced. ***  ,
Effects of negative-pressure wound therapy combinedwith microplasma on treating wounds of ulcer and the expression of heat shock protein 90
Authors: Wenxin Mi
Zhihong Li
Qihong Wang
Fei Gao
Yindong Ma
Mei Han
Guangyan Niu
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: angiogenesis; blood perfusion; heat shock protein 90; microplasma; negative-pressure wound therapy
Affiliations: Department of Burns Surgery, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China.

Abstract:  The effects of negative pressure wound therapy (NPWT) combined with microplasma on treating wounds of ulcer, and blood perfusion of wound-healing of interface, angiogenesis and the expressions of heat shock protein 90 (HSP90) were explored. We selected continuously 64 patients with wounds of ulcer. The patients were divided into the conventional treatment group (just medical foam dressing and 1% silver sulfadiazine cream for dressing changes) (n=20 cases), the NPWT group (n=22 cases) and the combination group (NPWT combined with microplasma) (n=22 cases), and compared the effects. It was found that in the 7 and 14 day combination group, maturity of granulation tissues and growth degree of epithelium were significantly higher than those in other two groups, and the areas of ulcer reduced significantly, the healing rate increased significantly (P&lt;0.05). In the 7 and 14 day combination group, blood perfusion of wounds and density of new vessels were significantly higher than the other two groups (P&lt;0.05). In the 7 and 14 day combination group, the expression of HSP90 was significantly higher than the other two groups (P&lt;0.05). In conclusion, NPWT combined with microplasma can improve the healing of woulds of ulcers, and it is related to the upregulated expression of HSP90. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader * Figure 1. Several panels appear to look unexpectedly similar, as shown here with boxes of the same color.  , 
 Figure 2: each panel resembles other panels, but in its own unique way. Several areas appear to be visible multiple times across panels.  ,
Synthetic control of FePtM nanorods (M = Cu, Ni) to enhance the oxygen reduction reaction
Authors: Shaojun Guo
Dong Su
Shouheng Sun
Sen Zhang
Huiyuan Zhu
Journal: Journal of the American Chemical Society (2013)
Discipline: CHEMISTRY
Keywords: nanocatalysts; oxygen reduction reaction; ternary alloy; FePtM; nanorods
Affiliations: Department of Chemistry, Brown University, Providence, Rhode Island 02912, United States, Center for Functional Nanomaterials, Brookhaven National Laboratory, Upton, New York 11973, United States

Abstract:  To further enhance the catalytic activity and durability of nanocatalysts for the oxygen reduction reaction (ORR), we synthesized a new class of 20 nm √ó 2 nm ternary alloy FePtM (M = Cu, Ni) nanorods (NRs) with controlled compositions. Supported on carbon support and treated with acetic acid as well as electrochemical etching, these FePtM NRs were converted into core/shell FePtM/Pt NRs. These core/shell NRs, especially FePtCu/Pt NRs, exhibited much improved ORR activity and durability. The Fe10Pt75Cu15 NRs showed a mass current densities of 1.034 A/mgPt at 512 mV vs Ag/AgCl and 0.222 A/mgPt at 557 mV vs Ag/AgCl, which are much higher than those for a commercial Pt catalyst (0.138 and 0.035 A/mgPt, respectively). Our controlled synthesis provides a general approach to core/shell NRs with enhanced catalysis for the ORR or other chemical reactions. 

Retracted: No

PubPeer comments:
 In Figure S3, the XRD patterns for the FePtNi with different composition ratio is totally same (even with noise bumps). Can the author check how this happened?  , 
 To Triplophyllum dicksonioide: First, the XRD patterns of FePtNi and FePtCu are very similar because after doping a third component (Ni, Cu), the trimetallic structure form a much more similar crystal phase than bimetallic FePt itself. Considering the small difference between the lattice parameters of Ni and Cu, the XRD instrumentation we used wasn t able to capture the subtle difference between those two. Regarding the statement of the noisy bumps are the same. We can t agree. These bumps are not noisy signals. In fact, they re peaks that were not fully revealed by the XRD (due to the limit of resolution). For example, the bump after 75 and before 90 can be attributed to (311) while the bumps around 69 and 47 can be attributed to (220) and (200) of the fcc structure. After doping with Cu or Ni, some subphases may emerge. For example, locally ordered L10 could be formed, leading to the appearance of bumps around 33 ((110), and double bumps around 50-53 ((201), (002)). Especially, tremendous literature discussed that doping Fe with a third component would promote the formation of ordered phases. However, with the limit of the XRD, those subphases appeared to be bumps in the spectra. To sum up, 1. FePtNi and FePtCu are very similar and more alike than their bimetallic counterpart FePt. 2. The noise mentioned by you is not noise. They are actually peaks that were not fully shown with the XRD. ,
Lightness matching and perceptual similarity
Authors: Anudhi P Munasinghe
Richard F Murray
Khushbu Y Patel
Journal: Journal of Vision (2018)
Discipline: CLINICAL MEDICINE
Keywords: Lightness constancy; surface reflectance; lighting intensity; discounting; perceptual similarity metric
Affiliations: Department of Psychology and Centre for Vision Research, York University, Toronto, Canada, , Department of Psychological and Brain Sciences, University of California, Santa Barbara, CA, USA, ://www.yorku.ca/rfm

Abstract:  Lightness constancy is the ability to perceive surface reflectance correctly despite substantial changes in lighting intensity. A classic view is that lightness constancy is the result of a "discounting" of lighting intensity, and this continues to be a prominent view today. Logvinenko and Maloney (2006) have proposed an alternative approach to understanding lightness constancy, in which observers do not make explicit estimates of reflectance, and lightness constancy is instead based on a perceptual similarity metric that depends on both the reflectance and the illuminance of surfaces viewed under different lighting conditions. Here we compare these two views using a novel, free-adjustment reflectance-matching task. We test whether observers can match reflectance in a task where they are free to adjust both the illuminance and the reflectance of the match stimulus over a wide range. We find that observers can match reflectance under these conditions, which supports the view that observers make explicit estimates of reflectance. We also compare performance in this free adjustment task using physical objects and computer-rendered images as stimuli. We find that lightness constancy is good in both cases, but with some evidence of a glow-related artifact with computer-rendered stimuli. 

Retracted: No

PubPeer comments:
 Figure 5B. Much more similar than expected.  , 
 Thank you for bringing this to attention These photomicrographs were not generated in my laboratory ,
MiR-92a regulates oral squamous cell carcinoma (OSCC) cell growth by targeting FOXP1 expression
Authors: Xiaohang Guan
Ning Wen
Sefei Yang
Song Cang
Jun Guo
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cell proliferation; FOXP1; MiR-92a; MicroRNAs; Oral squamous cell carcinoma.

Abstract:  Increasing evidence indicates that microRNAs dysregulation contributes to the development and progression of various human cancers, including oral squamous cell carcinoma (OSCC). However, little is known about the potential role of microRNA-92a (miR-92a) in OSCC. Thus, the aim of this study was to investigate the effects of miR-92a expression on OSCC cell growth, apoptosis and tumorigenesis. Real-time quantitative polymerase chain reaction was used to detect the expression level of miR-92a in primary tumor tissues and OSCC cell lines. The effects of miR-92a on cell proliferation, cell cycle, apoptosis and tumorigenesis of OSCC cells were explored after miR-92a expression was increased or decreased in the UM1 and Tca-8113 cells, respectively. The 3'-untranslated region (3'-UTR) of FOXP1 combined with miR-92a was analyzed with dual-luciferase reporter assays. The level of miR-92a expression was significantly up-regulated in the OSCC tissues and cell lines. The up-regulation of miR-92a expression promoted UM1 cell proliferation, cell cycle progression in vitro and tumor growth in nude mice, but its expression reduction inhibited these processes and induced apoptosis in Tca-8113 cells. Additionally, miR-92a expression was inversely correlated with FOXP1 protein expression in the OSCC tissues and cell lines. Furthermore, FOXP1 was identified as a functional downstream target of miR-92a by directly targeting the 3'-UTR of FOXP1. These findings indicate that miR-92a may act as a tumor inducer in OSCC by suppressing FOXP1 expression, and it could serve as a potential therapeutic target for OSCC treatment. 

Retracted: No

PubPeer comments:
 Fig. 4.  Effects of miR-92a on apoptosis in UM1 and Tca-8113 cells. Apoptotic cells were detected using Annexin V-FITC PI apoptosis detection kit and flow cytometry after transfection with miR-92a mimics or inhibitor into UM1 or Tca-8113 cells.  Controls for UM1 and Tca-8113 are more similar than one would expect, especially in the lower left quadrants. Here highlighted by superimposing the two panels, after black white reversing the Tca-8113 control so that identical points cancel out.  ,
Butyric Acid Protects Against Renal Ischemia‚ÄìReperfusion Injury by Adjusting the Treg/Th17 Balance via HO-1/p-STAT3 Signaling
Authors: Lianghua Jiang
Jian Shi
Miaomiao Wang
Yunjie Lu
Tianhao Ji
Zhen Chen
Shikun Yang
Jing Chen
Wei Ding
Zhiwen Fan
Journal: Frontiers in Cell and Developmental Biology (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HO-1; STAT3; Th17; Treg; butyric acid
Affiliations: The Third Affiliated Hospital of Soochow University, Changzhou, China., Key Laboratory of Liver Transplantation, Hepatobiliary/Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, China., The First People's Hospital of Kunshan, Kunshan, China., Department of Pathology, Affiliated Nanjing Drum Tower Hospital of Nanjing University School of Medicine, Nanjing, China.

Abstract:  Immune regulation plays a vital role in ischemia-reperfusion injury (IRI). Butyric acid (BA) has immunomodulatory effects in many diseases, but its immunomodulatory effects during renal IRI are still unclear. Our research shows that BA protected against IRI and significantly improved renal IRI in vivo. In vitro studies showed that BA inhibits Th17 cell differentiation and induces Treg cell differentiation. Mechanism studies have shown that heme oxygenase 1 (HO-1)/STAT3 signaling pathway was involved in the inhibitory effect of BA on Th17 cell differentiation. HO-1 inhibitors can significantly rescue the BA-mediated inhibition of Th17 cell differentiation. We confirmed that BA promotes the differentiation of Th17 cells into Treg cells by regulating the pathway and reduces renal IRI. 

Retracted: No

PubPeer comments:
 Several paragraphs of this article (Figure 1 to 4) were republished with the same words in English into the article entitled  Aiming for zero fluid accumulation: First, do no harm , published by Anaesthesiology Intensive Therapy 2021;53(2):162-178. doi: 10.5114 ait.2021.105252. (Figure 5). Several of the authors participated in both articles. The article published by the Revista Chilena de Anestesia was received on 04 12 2021, which was one day before the article published in the Anesthesiology Intensive Therapy journal was accepted (04 13 2021). The authors intended (and managed) to deliberately publish part of the content of their articles in different languages. Figure 1  Figure 2  Figure 3  Figure 4  Figure 5  ,
Alteration of the methylation status of tumor-promoting genes decreases prostate cancer cell invasiveness and tumorigenesis in vitro and in vivo
Authors: Nicholas Shukeir
Moshe Szyf
Gaoping Chen
Shafaat A Rabbani
Pouya Pakneshan
Journal: Cancer Research (2006)
Discipline: CLINICAL MEDICINE
Keywords: cell invasiveness; tumorigenesis; hypomethylation; genes; tumor progression
Affiliations: Department of Medicine, McGill University, Montreal, Quebec, Canada.

Abstract:  We tested the hypothesis that cell invasiveness and tumorigenesis are driven by hypomethylation of genes involved in tumor progression. Highly invasive human prostate cancer cells PC-3 were treated with either the methyl donor S-adenosylmethionine (SAM) or methyl DNA-binding domain protein 2 antisense oligonucleotide (MBD2-AS). Both treatments resulted in a dose- and time-dependent inhibition of key genes, such as urokinase-type plasminogen activator (uPA), matrix metalloproteinase-2 (MMP-2), and vascular endothelial growth factor expression to decrease tumor cell invasion in vitro. No change in the levels of expression of genes already known to be methylated in late-stage prostate cancer cells, such as glutathione S-transferase P1 and androgen receptor, was seen. Inoculation of PC-3 cells pretreated with SAM and MBD2-AS into the flank of male BALB/c nu/nu mice resulted in the development of tumors of significantly smaller volume compared with animals inoculated with PC-3 cells treated with vehicle alone or MBD2 scrambled oligonucleotide. Immunohistochemical analysis of tumors showed the ability of SAM and MBD2-AS to significantly decrease tumoral uPA and MMP-2 expression along with levels of angiogenesis and survival pathway signaling molecules. Bisulfite sequencing analysis of tumoral genomic DNA showed that inhibition of both uPA and MMP-2 expression was due to methylation of their 5' regulatory region. These studies support the hypothesis that DNA hypomethylation controls the activation of multiple tumor-promoting genes and provide valuable insight into developing novel therapeutic strategies against this common disease, which target the demethylation machinery. 

Retracted: No

PubPeer comments:
null, 
 #1 Came across this independently. Figure 2B. Much more similar than expected.  , 
 Figure 5A. Much more similar than expected.  , 
 Figures 1A and 2A. Much more similar than expected.  ,
Regulation of Reactionary Dentine Formation
Authors: P T Sharpe
V C M Neves
Journal: Journal of Dental Research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Wnt signalling; growth factors; matrix organization; odontoblast; repair
Affiliations: 1 Centre for Craniofacial and Regenerative Biology, Dental Institute, Kings College London, UK.

Abstract:  During the treatment of dental caries that has not penetrated the tooth pulp, maintenance of as much unaffected dentine as possible is a major goal during the physical removal of decayed mineral. Damage to dentine leads to release of fossilized factors (transforming growth factor-Œ≤ [TGF-Œ≤] and bone morphogenic protein [BMP]) in the dentine that are believed to stimulate odontoblasts to secrete new "tertiary" dentine (reactionary dentine). This is formed on the pulpal surface of existing dentine and rethickens the dentine. We have previously shown that activation of Wnt/Œ≤-catenin signaling is pivotal for tooth repair in exposed pulp injury, and the pathway can be activated by small-molecule GSK-3 antagonists, resulting in enhanced reparative dentine formation. Here, we use a nonexposed pulp injury model to investigate the mechanisms of reactionary dentine formation in vivo, using small molecules to modulate the Wnt/Œ≤-catenin, TGF-Œ≤, and BMP pathways. We found that a local increase of Wnt activation at the injury site enhances reactionary dentine secretion. In addition, inhibition of TGF-Œ≤, BMP, or Wnt pathways does not impede reactionary dentine formation, although inhibition of TGF-Œ≤ and/or BMP signaling does result in more disorganized, nontubular reactionary dentine. This suggests that Wnt/Œ≤-catenin signaling plays no major role in the formation of reactionary dentine, but in common with reparative dentine formation, exogenous elevation of Wnt/Œ≤-catenin signaling can enhance tertiary dentine formation. Release of latent TGF-Œ≤ or BMPs from dentine is not required for the deposition of mineral to form reactionary dentine but does play a role in its organization. 

Retracted: No

PubPeer comments:
 Two images in Figure 2 appear to overlap at different magnification (red boxes). ***  ,
The roles of hypoxia-inducible Factor-1 and iron regulatory protein 1 in iron uptake induced by acute hypoxia
Authors: Li Zhu
Xue-Ting Wang
Lei Yang
Ya-Peng Lu
Dan Wang
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Divalent metal transporter 1; Hypoxia-inducible factor 1Œ±; Iron regulatory protein 1; Iron uptake; Transferrin receptor 1.
Affiliations: Department of Biochemistry, Institute for Nautical Medicine, Nantong University, Nantong, 226019, China., Department of Biochemistry, Institute for Nautical Medicine, Nantong University, Nantong, 226019, China. Electronic address: .

Abstract:  Background information: Divalent metal transporter 1 (DMT1) and transferrin receptor (TfR1) are vital proteins for cellular iron uptake. These proteins have hypoxia-responsive elements (HREs) in their 5'-regulatory region, and they are regulated by hypoxia-inducible factor 1Œ± (HIF-1Œ±) transcriptionally under hypoxic condition. Besides, iron regulatory protein 1 (IRP1) regulates DMT1 and TfR1 by binding to iron-responsive elements (IREs) present in their mRNAs to control cellular iron homeostasis. Results: Here, we explored the effect of acute hypoxia on iron uptake. Ferrous iron uptake was elevated by DMT1(+IRE) and TfR1 under acute hypoxia. The luciferase activity analysis revealed that the functional HREs of DMT1 and TfR1 were increased. However, their IREs-dependent luciferase activities were reduced simultaneously. The mRNA stability of TfR1 and DMT1(+IRE) was suppressed under acute hypoxia. The mRNA levels of TfR1 and DMT1(+IRE) were restrain by silencing IRP1. In sharp contrast, HIF-1Œ± overexpression enhanced the mRNA levels of TfR1 and DMT1(+IRE), which reversed the inhibition of IRP1 on both. HIF-1Œ± konckdown suppressed the hypoxia-induced increase expression of TfR1 and DMT1(+IRE), whereas both proteins had little change when further decreased the IRP1 expression under hypoxia. Hypoxia upregulated the protein expression of Ferrtin-L in a time-dependent manner, yet there was no different when IRP1 silencing or overexperssion under hypoxia. The lactate dehydrogenase (LDH) release induced by hypoxia was increased by TfR1 siRNA silence. Conclusions: We propose that HIF-1/HRE system might play a principal part in hypoxia induced iron uptake. 

Retracted: No

PubPeer comments:
 Figure 3A appears to have a repeated band, after altering dimensions. ***  ,