PReD-Bench/PRed-Bench huggingface dataset:
Clinical efficacy and prognosis of aspirin combined with clopidogrel in patients with cerebral hemorrhage after operation
Authors: W-L Ding
X-J Guo
H-H Zhu
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: hypertensive cerebral hemorrhage; aspirin; clopidogrel; decompressive craniectomy; intracranial hematoma
Affiliations: Department of Emergency, Affiliated Hospital of Jining Medical University, Jining, P.R. China. .

Abstract:  Objective: The aim of this study was to investigate clinical effect, the quality of life, and prognosis of patients with hypertensive cerebral hemorrhage treated with aspirin combined with clopidogrel after decompressive craniectomy and removal of intracranial hematoma. Patients and methods: The individual patient data of 120 patients with hypertensive cerebral hemorrhage admitted to Affiliated Hospital of Jining Medical University from January 2015 to July 2016 were retrospectively analyzed. The patients were divided into a research group (62 cases) and a control group (58 cases). The control group was treated with aspirin, while the research group was treated with aspirin combined with clopidogrel. The prevalence of adverse reactions was compared between the two groups. Activity of daily living (ADL) was used to evaluate the quality of life. The amount of hematoma before and after operation was compared between the two groups. The prognosis of the two groups and the risk factors of postoperative rebleeding in patients with cerebral hemorrhage were analyzed. Results: The prevalence of adverse reactions in the research group was significantly higher than that in the control group (p&lt;0.05). The ADL scores of both groups 14 days after the operation were higher than those before the operation (p&lt;0.05), and the ADL scores of the research group were significantly lower than those of the control group 14 d after the operation (p&lt;0.05). The amount of hematoma in the two groups after surgery was lower than that before surgery (p&lt;0.05), and the amount of hematoma in the research group was higher than that in the control group (p&lt;0.05). Conclusions: The combination of aspirin and clopidogrel will increase the prevalence of adverse reactions and reduce the quality of life of patients after decompressive craniectomy and removal of intracranial hematoma in patients with hypertensive intracerebral hemorrhage. Careful medication is required in clinic. 

Retracted: Yes

PubPeer comments:
 Withdrawn. The journal does not provide any details beyond  This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. ,
S100Œ≤ as a biomarker for differential diagnosis of intracerebral hemorrhage and ischemic stroke
Authors: Yiping Wang
Saijun Zhou
Jianhong Bao
Suyue Pan
Journal: Neurological research (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Biomarker; Hemorrhage; NIHSS; S100Œ≤; Stroke.
Affiliations: a Department of Neurology, Nanfang Hospital , Southern Medical University , Guangzhou , China., b Department of Neurology , The 1st Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.

Abstract:  Objective: To explore the efficacy of S100 calcium-binding protein B (S100Œ≤) in differentiating between intracerebral hemorrhage (ICH) and ischemic stroke (IS). Methods: From June 2014 to July 2015, 46 ICH and 71 IS patients who had undergone computed tomography (CT) scans were enrolled. Patients' neurological deficits were evaluated by the National Institutes of Health stroke scale (NIHSS), and the modified Rankin scale (mRS) was used to assess functional disability 90 days after discharge. Plasma S100Œ≤ was measured from a blood sample drawn upon arrival at the emergency department. Results: The plasma S100Œ≤ concentration in the ICH group was significantly higher than in the IS group (p &lt; 0.001). There were only significant correlations between S100Œ≤ and hemorrhage volume (r = 0.820, p &lt; 0.001), NIHSS score (r = 0.389, p = 0.008), and mRS (r = 0.732, p &lt; 0.001) in the ICH group. Furthermore, receiver-operating characteristic (ROC) curve analysis revealed that an S100Œ≤ concentration of 67 pg/ml yielded an area under the curve (AUC) of 0.903 with 95.7% sensitivity and 70.4% specificity in differentiating between ICH and IS. In the ICH group, the plasma S100Œ≤ concentration was significantly elevated in patients with poor functional outcome vs. those with favorable functional outcome (p &lt; 0.001). ROC curve analysis showed that an S100Œ≤ concentration of 133 pg/ml yielded an AUC of 0.924 with 100% sensitivity and 76.2% specificity in identifying ICH patients with poor functional outcome. Conclusion: S100Œ≤ could serve as a potential biomarker for differentiating between ICH and IS and predicting short-term functional outcome after ICH. 

Retracted: No

PubPeer comments:
 The content, and especially the results that are presented in this article are highly similar to the results reported by Xiong et al. (2015) in Neurological Sciences , although Zhou et al. report that they studied S100b, while Xiong et al. studied GFAP. Zhou et al. reported a slightly higher number of patients in each group, but with almost identical characteristics as reported by Xiong et al. even though the materials and methods of both papers describe the cohorts to have been established in different, non-overlapping time periods, as well as at different hospitals.  *Left: Zhou et al. (2016), Right: Xiong et al. (2015)* Also the figures, especially figures 2 (correlation plots with NIHSS scores) and figures 3 (ROC curve analysis) are highly similar, casting doubts on the authenticity of the paper. ,
Apoptosis induction and inhibition of hyperplasia formation by 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]-2H-benzo(b)pyran in rat uterus
Authors: Vishal Chandra
Iram Fatima
Sharad Sharma
Mohammad Kamil Hussain
Shakti Kitchlu
Kanchan Hajela
Preeti Bajpai
Anila Dwivedi
Ruchi Saxena
Journal: American Journal of Obstetrics and Gynecology (2011)
Discipline: CLINICAL MEDICINE
Keywords: antiproliferative mechanism; estradiol-induced rat uterine hyperplasia; K-1; apoptosis; Akt activation
Affiliations: Division of Endocrinology, Central Drug Research Institute, Council of Scientific and Industrial Research, Lucknow, India.

Abstract:  Objective: The study was undertaken to explore the antiproliferative mechanism of action of 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]-2H-benzo(b)pyran (K-1) in estradiol-induced rat uterine hyperplasia. Study design: Adult ovariectomized rats received vehicle or estradiol alone (20 Œºg/kg) or estradiol along with K-1 (100 or 200 Œºg/kg) for 14 days. Uterine histomorphometric analysis and immunoblotting were performed. Caspase-3 activity and terminal deoxynucleotidyl transferase-mediated nick end-labeling staining were performed to analyze the apoptotic potential of compound. Results: Compound inhibited estradiol-induced uterine weight and histomorphometric changes pertaining to endometrial growth and down-regulated the expression of estrogen response element and activator protein-1 regulated genes and transcription factors. The compound significantly induced apoptosis, interfered with Akt activation, decreased X-linked inhibitor of apoptosis protein expression leading to an increased cleavage of caspase-9, caspase-3, poly(adenosine diphosphate-ribose) polymerase, increased Bax/Bcl2 ratio, and caspase-3 activity. Conclusion: K-1 inhibits endometrial proliferation via nonclassical estrogen receptor signaling mechanisms. It interfered with Akt activation and induced apoptosis via the intrinsic pathway and inhibited estradiol-induced hyperplasia formation in rat uterus. 

Retracted: No

PubPeer comments:
 Unexpected similarities in the b-actin panels of Figure 3B and Figure 4A. Although the first 2 lanes appear to describe the same samples, the right 2 lanes supposedly are different experiments. Highlighted with red boxes:  , 
 #1 I am very much grateful to you for indicating the inadvertent error in the manuscript. The article is discussing only about a single compound (2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]-2H-benzo(b)pyran) i. e. K-1. Initially, we named this compound as Drug 2 oru2018D2u2019, later, we re-named it as K-1 based on the name of the chemist. So D-2 and K-1 are denoting the same compound. Therefore, bands including beta actin presented in Figure 3B and Figure 4A came from the same blot developed from same compound treatment. I guess there is no confusion now. We apologize for this inadvertent mistake. We are submitting an erratum to the journal. Best, ,
Functional characterization of the long noncoding RNA MIR22HG as a tumour suppressor in cervical cancer by targeting IGF2BP2
Authors: D Wang
J Shu
Journal: European Review for Medical and Pharmacological Sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cervical cancer; MIR22HG; tumour suppressor; lincRNA; metastasis
Affiliations: Key Laboratory for Biorheological Science and Technology of Ministry of Education (Chongqing University), Chongqing University Cancer Hospital, Chongqing, China. .

Abstract:  Objective: Cervical cancer is the most common malignant tumour in the female reproductive tract, ranking second in the global cause of female cancer and seriously endangering women's health. However, the underlying mechanisms leading to cervical cancer are unclear. Previous studies have reported the roles and general underlying mechanisms of the long noncoding RNA MIR22HG (MIR22HG) in multiple types of tumours. Patients and methods: In this study, we describe the functional role of MIR22HG as a tumour suppressor lincRNA by regulating metastasis, growth and invasion by performing a series of in vivo and in vitro experiments. Results: Our data suggested that MIR22HG dramatically promoted cervical cancer apoptosis and inhibited invasion by targeting IGF2BP2. Conclusions: The long noncoding RNA MIR22HG targets IGF2BP2 as a tumour suppressor in cervical cancer. Our findings will be helpful for developing potential therapeutics for cervical cancer. 

Retracted: No

PubPeer comments:
 Figure 2B: * Boxes in shades of red: Some groups of dots look remarkably similar across the three panels Figure 5B: * Boxes in shades of blue: Some groups of dots look remarkably similar across the three panels  , 
 Table 1. * The percentages given in the right-most column appear to be completely off. 42 50 is 84%, not 92.54. 8 40 is 16% , not 7.46, etc. * 12 of the 50 cervical cancer patients were HPV negative, which is unexpectedly high, since HPV is the causative agent for nearly all cervical cancers. HPV-negative cervical cancer has been reported, but the percentage is usually in the 10% range, and 24% is just very high and unexpected. See e.g. https: www.ncbi.nlm.nih.gov pmc articles PMC6516188 Which HPV detection methods was used here? I hope that the Key Laboratory of Biorheological Science will be able to give more background here.  ,
Galunisertib inhibits glioma vasculogenic mimicry formation induced by astrocytes
Authors: Bin Huang
Aanjing Chen
Ying He
Chao Zhang
Jian Wang
Xin Zhang
Wenliang Chen
Xingang Li
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Gliomas; Vasculogenic mimicry; Astrocytes; TGF-Œ≤1; Galunisertib
Affiliations: Department of Neurosurgery, Qilu Hospital, Shandong University, 107 Wenhuaxi Road, Jinan, China., Brain Science Research Institute, Shandong University, 44 Wenhuaxi Road, Jinan, China., Institute of Basic Medical Sciences and Key Laboratory of Cardiovascular Proteomics of Shandong Province, Qilu Hospital, Shandong University, 44 Wenhuaxi Road, Jinan, China., Department of Biomedicine, University of Bergen, Jonas Lies Vei 91, 5009-Bergen, Norway.

Abstract:  Gliomas are among the most lethal primary brain tumors found in humans. In high-grade gliomas, vasculogenic mimicry is often detected and has been correlated with prognosis, thus suggesting its potential as a therapeutic target. Vasculogenic mimicry mainly forms vascular-like channels independent of endothelial cells; however, little is known about the relationship between astrocytes and vasculogenic mimicry. In our study, we demonstrated that the presence of astrocytes promoted vasculogenic mimicry. With suspension microarray technology and in vitro tube formation assays, we identified that astrocytes relied on TGF-Œ≤1 to enhance vasculogenic mimicry. We also found that vasculogenic mimicry was inhibited by galunisertib, a promising TGF-Œ≤1 inhibitor currently being studied in an ongoing trial in glioma patients. The inhibition was partially attributed to a decrease in autophagy after galunisertib treatment. Moreover, we observed a decrease in VE-cadherin and smooth muscle actin-Œ± expression, as well as down-regulation of Akt and Flk phosphorylation in galunisertib-treated glioma cells. By comparing tumor weight and volume in a xenograft model, we acquired promising results to support our theory. This study expands our understanding of the role of astrocytes in gliomas and demonstrates that galunisertib inhibits glioma vasculogenic mimicry induced by astrocytes. 

Retracted: No

PubPeer comments:
 The micrographs in this papers seem to be randomly organized into panels to make up a story. There are several cases in Figure 1G, 2A, 2F and 4D where micrographs have been duplicated and presented as something else. In some cases they have apparently also been manipulted.  ,
lncRNA ZEB2-AS1 Aggravates Progression of Non-Small Cell Lung Carcinoma via Suppressing PTEN Level
Authors: Kangwu Wang
Xiao Chen
Journal: Medical Science Monitor (2019)
Discipline: CLINICAL MEDICINE
Keywords: lncRNA ZEB2-AS1; NSCLC development; PTEN; EZH2; tumor staging
Affiliations: Department of Gerontology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China (mainland)., Department of Thoracic Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China (mainland).

Abstract:  BACKGROUND The aim of this study was to assess the involvement of lncRNA ZEB2-AS1 in the development of NSCLC and to explore the potential mechanism involved. MATERIAL AND METHODS ZEB2-AS1 expressions in 48 paired NSCLC tissues and paracancerous tissues were examined by qRT-PCR. ZEB2-AS1 level in NSCLC patients affected by tumor staging and lymphatic metastasis was examined as well. Regulatory effects of ZEB2-AS1 on proliferative, migratory, and invasive properties of NCI-H1650 and HCC827 cells were evaluated. The interaction between ZEB2-AS1 and EZH2 was identified through RIP assay. Subsequently, the binding of EZH2 on PTEN promoter region was tested by ChIP. Finally, rescue experiments were conducted to assess the involvement of PTEN in the development of NSCLC. RESULTS ZEB2-AS1 was upregulated in NSCLC tissues and cell lines. Its level was higher in NSCLC patients with T3-T4 or accompanied with lymphatic metastasis relative to those with T1-T2 or without metastatic loci. Knockdown of ZEB2-AS1 suppressed proliferative, migratory, and invasive properties of NCI-H1650 and HCC827 cells. PTEN level was elevated after knockdown of ZEB2-AS1 or EZH2 in HCC827 cells. Subsequently, RIP assay proved the interaction between ZEB2-AS1 and EZH2. Knockdown of ZEB2-AS1 markedly reduced the binding of EZH2 on the PTEN promoter region. Notably, knockdown of PTEN reversed the effects of EZB2-AS1 on regulating proliferative, migratory, and invasive properties of NSCLC cells. CONCLUSIONS lncRNA ZEB2-AS1 is upregulated in NSCLC, which elevates the viability and malignant degree of NSCLC cells by downregulating PTEN, thus aggravating the progression of NSCLC. 

Retracted: No

PubPeer comments:
 Fig. 2D. Unexpectedly similar.  , 
 Figure 3A contains a set of WB images which appear more similar than expected, after one band exposed to horizontal flipping.  , 
 Thanks for pointing these out. We are currently checking the original data of these Figures, and also repeating the experiments. ,
Inhibition of S6 kinase suppresses the apoptotic effect of eIF4E ablation by inducing TGF-Œ≤-dependent G1 cell cycle arrest
Authors: David A Foster
Paige Yellen
Angela Preda
Amrita Chatterjee
Journal: Cancer Letters (2013)
Discipline: CLINICAL MEDICINE
Keywords: mTORC1; translation; apoptosis; eIF4E; S6 kinase
Affiliations: Department of Biological Sciences, Hunter College of The City University of New York, 695 Park Avenue, New York, NY 10065, USA.

Abstract:  The mammalian target of rapamycin complex 1 (mTORC1) is a critical regulator of cap-dependent translation through its direct activation of ribosomal protein p70 S6 kinase (S6 kinase) and indirect activation of eukaryotic initiation factor 4E (eIF4E). We recently reported that inhibition of eIF4E expression caused apoptosis in cancer cells in the absence of serum. This was indicated by treatment with the mTORC1 inhibitor rapamycin, which suppressed both S6 kinase and 4E-BP1 phosphorylation (dephosphorylated 4E-BP1 binds and inactivates eIF4E), or by knockdown of eIF4E. We report here that knockdown of eIF4E also causes apoptosis in the presence of serum. This was unexpected because rapamycin induces G1 cell cycle arrest in the presence of serum. Upon investigation, we have found that inactivated S6 kinase prevents the apoptotic effect observed by singular knockdown of eIF4E and results in G1 cell cycle arrest. This effect is dependent on TGF-Œ≤ (transforming growth factor-Œ≤) signaling which contributes to G1 cell cycle arrest. Suppression of S6 kinase phosphorylation alone is insufficient to mediate cell cycle arrest, indicating that complete G1 cell cycle arrest is due to suppression of both S6 kinase and eIF4E. These data indicate that the cytostatic effect of rapamycin is suppression of both S6 kinase and eIF4E, while the cytotoxic effects are due suppression of eIF4E in the absence of S6 kinase-dependent activation of TGF-Œ≤ signals. Our findings place an importance on the evaluating the activity/expression level of S6 kinase and eIF4E as readouts for rapamycin/rapalog efficacy. 

Retracted: No

PubPeer comments:
 Figure 2C. Splices in 2 panels, but no in the other panel.  ,
Sex differences in the cerebellum and frontal cortex: roles of estrogen receptor alpha and sex chromosome genes
Authors: Jean M Abel
Diane M Witt
Emilie F Rissman
Journal: Neuroendocrinology (2011)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: neurobehavioral diseases; sexually dimorphic; Calbindin D28K; hypothalamus; C56BL/6J mice
Affiliations: Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.

Abstract:  Most neurobehavioral diseases are sexually dimorphic in their incidence, and sex differences in the brain may be key for understanding and treating these diseases. Calbindin (Calb) D28K is used as a biomarker for the well-studied sexually dimorphic nucleus, a hypothalamic structure that is larger in males than in females. In the current study weanling C56BL/6J mice were used to examine sex differences in the Calb protein and message focusing on regions outside of the hypothalamus. A robust sex difference was found in Calb in the frontal cortex (FC) and cerebellum (CB; specifically in Purkinje cells); mRNA and protein were higher in females than in males. Using 2 mouse lines, i.e. one with a complete deletion of estrogen receptor alpha (ERŒ±) and the other with uncoupled gonads and sex chromosomes, we probed the mechanisms that underlie sexual dimorphisms. In the FC, deletion of ERŒ± reduced Calb1 mRNA in females compared to males. In addition, females with XY sex chromosomes had levels of Calb1 equal to those of males. Thus, both ERŒ± and the sex chromosome complement regulate Calb1 in the FC. In the CB, ERŒ± knockout mice of both sexes had reduced Calb1 mRNA, yet sex differences were retained. However, the sex chromosome complement, regardless of gonadal sex, dictated Calb1 mRNA levels. Mice with XX chromosomes had significantly greater Calb1 than did XY mice. This is the first study demonstrating that sex chromosome genes are a driving force producing sex differences in the CB and FC, which are neuoranatomical regions involved in many normal functions and in neurobehavioral diseases. 

Retracted: No

PubPeer comments:
 Hello In the methods the authors write:  The intensities of Calb and actin on individual films were measured and analyzed by densitometry with Im- ageQuant (GE Healthcare Life Sciences). Levels of Calb were normalized to those of actin in each sample and the protein amount was expressed as the ratio of calbindin to actin. Five brains from each sex were used for these blots. However in figure 2 we cannot see any actin from the blots  ,
Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19
Authors: Christian Unge
David J Wullimann
Efthymia Kokkinou
Olav Rooyackers
Susanna Brighenti
Karolinska COVID-19 Study Group
Takuya Sekine
Magalini Lourda
Annika Olsson
Tobias Kammann
Lena Berglin
Mira Akber
Elizabeth Henriksson
Emma Ringqvist
Johan M√•rtensson
Jakob Michaelsson
Bj√∂rn Persson
Johan K Sandberg
Egle Kvedaraite
Jean-Baptiste Gorin
Alvaro Haroun-Izquierdo
Benedict Chambers
Sian Llewellyn-Lacey
Lena Radler
Sandra Muschiol
Hedvig Glans
Nicole Marquardt
Malin Flodstr√∂m Tullberg
Jan Albert
Kimia Maleki
Lena Dillner
Andreas Von Kries
Laura Palma Medina
Johanna Emg√•rd
Christopher Maucourant
Anders S√∂nnerborg
Isabel Diaz Lozano
Tiphaine Parrot
Habiba Kamal
Sadaf Kalsum
Angelica Cuapio Gomez
Marta Butrym
Sara Gredmark-Russ
Morten Nielsen
Andr√© Perez-Potti
Majda Dzidic
Jagadees Muva
Tea Soini
Gordana Bogdanovic
Soo Aleman
Kristoffer Str√•lin
Elin Folkesson
Olga Rivera-Ballesteros
Jan-Inge Henter
Jonas Klingstr√∂m
Tobias Allander
Mattias Svensson
Kirsten Moll
Lars I Eriksson
John Tyler Sandberg
Pontus Naucl√©r
Jonathan Grip
Puran Chen
Ebba Sohlberg
Niklas K Bj√∂rkstr√∂m
Hans-Gustaf Ljunggren
Helena Bergsten
Demi Brownlie
Martin Cornillet Jeannin
Anna F√§rnert
Janne Tynell
Karl-Johan Malmberg
Jenny Mj√∂sberg
Laura Hertwig
Marco Loreti
Anna Norrby-Teglund
Renata Varnaite
David A Price
Marcus Buggert
Journal: Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SARS-CoV-2-specific memory T cells; immune protection; COVID-19; functional landscape; phenotypic landscape

Abstract:  SARS-CoV-2-specific memory T cells will likely prove critical for long-term immune protection against COVID-19. Here, we systematically mapped the functional and phenotypic landscape of SARS-CoV-2-specific T cell responses in unexposed individuals, exposed family members, and individuals with acute or convalescent COVID-19. Acute-phase SARS-CoV-2-specific T cells displayed a highly activated cytotoxic phenotype that correlated with various clinical markers of disease severity, whereas convalescent-phase SARS-CoV-2-specific T cells were polyfunctional and displayed a stem-like memory phenotype. Importantly, SARS-CoV-2-specific T cells were detectable in antibody-seronegative exposed family members and convalescent individuals with a history of asymptomatic and mild COVID-19. Our collective dataset shows that SARS-CoV-2 elicits broadly directed and functionally replete memory T cell responses, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19. 

Retracted: No

PubPeer comments:
 Figure 8 shows two identical patterns for sample before and after adsorption ,
MicroRNA-375 accelerates the invasion and migration of colorectal cancer through targeting RECK
Authors: D-M Bai
Z-Y Wang
L-J Wei
B-C Liu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-375; colorectal cancer; progression; expression pattern; regulatory mechanism
Affiliations: Department of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Changchun, China. .

Abstract:  Objective: This study aims to detect the expression pattern of microRNA-375 in colorectal cancer (CRC), and to examine its specific mechanism in regulating the progression of CRC. Patients and methods: We detected microRNA-375 expression in 50 pairs of CRC and paracancerous tissues by quantitative real-time polymerase chain reaction (qRT-PCR). Correlation between microRNA-375 expression and pathological indexes of CRC patients was analyzed. Cellular expression of microRNA-375 in CRC cell lines was detected as well. Regulatory effect of microRNA-375 on biological behaviors of CRC cells was examined, including proliferative, invasive and migratory abilities. We used bioinformatics method to predict the potential target of microRNA-375 and finally explored their interactive functions in regulating CRC progression. Results: MicroRNA-375 expression remained higher in CRC tissues relative to paracancerous ones. CRC patients with a high level of microRNA-375 tended to have higher rates of lymph node metastasis and distant metastasis compared with those with a low level. Transfection of microRNA-375 inhibitor greatly reduced proliferative, invasive and migratory abilities of CRC cells. RECK was predicted to be the target of microRNA-375, which was downregulated in CRC tissues and cells. Besides, RECK expression was negatively regulated by microRNA-375 in CRC. Rescue experiments confirmed that microRNA-375/RECK axis promoted the malignant progression of CRC. Conclusions: MicroRNA-375 is upregulated in CRC, and correlated to lymph node metastasis and distant metastasis. MicroRNA-375 enhances invasive and migratory abilities of CRC cells via regulating RECK. 

Retracted: No

PubPeer comments:
 Fig 3C.  A negative correlation between RECK and miR-375 in CRC (r2 =0.172, p 0.005, n=50) . Rescaled slightly for ease of comparison with (right) a superimposition of 20 versions of a single correlation scatterplot, from different papers. Data-points are darker if they appear in more of those 20 variants.  Here 3C (red) is superimposed on the composite to show that it derives from the same source.  Note also that the distribution of RECK expression in CRC tissues, shown on the horizontal axis of Fig 3C, does not seem to match the distribution shown in 3A.  Table 1. This form of incomplete Table 1, where the column headings promise to convert the number of patients into each subgroup into percentages but the table does not deliver, is common in papers in this journal.  ,
Synergistic growth inhibition of squamous cell carcinoma of the head and neck by erlotinib and epigallocatechin-3-gallate: the role of p53-dependent inhibition of nuclear factor-kappaB
Authors: Dong M Shin
Zhuo Georgia Chen
A R M Ruhul Amin
Fadlo R Khuri
Journal: Cancer Prevention Research (2009)
Discipline: CLINICAL MEDICINE
Keywords: green tea polyphenol; epigallocatechin-3-gallate; EGCG; epidermal growth factor receptor-tyrosine kinase inhibitor; erlotinib
Affiliations: Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, Georgia 30322, USA.

Abstract:  We have previously reported that the green tea polyphenol epigallocatechin-3-gallate (EGCG) and the epidermal growth factor receptor-tyrosine kinase inhibitor erlotinib had synergistic growth-inhibitory effects in cell culture and a nude mouse xenograft model of squamous cell carcinoma of the head and neck. However, the mechanism of their antitumor synergism is not fully understood. In the current study, we investigate the mechanism of their synergistic growth-inhibitory effects. The treatment of squamous cell carcinoma of the head and neck cell lines with erlotinib time-dependently increased the expression of cell cycle regulatory proteins p21 and p27 and apoptosis regulatory protein Bim. EGCG alone had very little or no effect on the expression of these proteins among the cell lines. However, simultaneous treatment with EGCG and erlotinib strongly inhibited erlotinib-induced expression of p21 and p27 without affecting the expression of Bim. Moreover, erlotinib increased the expression of p53 protein, the ablation of which by short hairpin RNA strongly inhibited EGCG- and erlotinib-mediated growth inhibition and the expression of p21, p27, and Bim. In addition, combined treatment with erlotinib and EGCG inhibited the protein level of p65 subunit of nuclear factor-kappaB and its transcriptional target Bcl-2, but failed to do so in cells with ablated p53. Taken together, our results, for the first time, suggest that erlotinib treatment activates p53, which plays a critical role in synergistic growth inhibition by erlotinib and EGCG via inhibiting nuclear factor-kappaB signaling pathway. Characterizing the underlying mechanisms of EGCG and erlotinib synergism will provide an important rationale for chemoprevention or treatment trials using this combination. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than you would expect. https: imgur.com sNYEFeH ,
A comparative analysis of Dmc1 and Rad51 nucleoprotein filaments
Authors: Robyn Roth
Michael G Sehorn
Sean D Sheridan
Xiong Yu
Douglas K Bishop
Patrick Sung
Edward H Egelman
John E Heuser
Journal: Nucleic acids research (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RecA homologs; Rad51; Dmc1; strand exchange; meiosis
Affiliations: Committee on Genetics, University of Chicago, Chicago, IL 60637, USA.

Abstract:  The eukaryotic RecA homologs Rad51 and Dmc1 are essential for strand exchange between homologous chromosomes during meiosis. All members of the RecA family of recombinases polymerize on DNA to form helical nucleoprotein filaments, which is the active form of the protein. Here we compare the filament structures of the Rad51 and Dmc1 proteins from both human and budding yeast. Previous studies of Dmc1 filaments suggested that they might be structurally distinct from filaments of other members of the RecA family, including Rad51. The data presented here indicate that Rad51 and Dmc1 filaments are essentially identical with respect to several structural parameters, including persistence length, helical pitch, filament diameter, DNA base pairs per helical turn and helical handedness. These data, together with previous studies demonstrating similar in vitro recombinase activity for Dmc1 and Rad51, support the view that differences in the meiotic function of Rad51 and Dmc1 are more likely to result from the influence of distinct sets of accessory proteins than from intrinsic differences in filament structure. 

Retracted: No

PubPeer comments:
 image duplication  Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. , 
 #1 The image duplication appears to have resulted from an inadvertent error made during figure preparation in my laboratory. The error, while regrettable, has no impact on the conclusions of the paper. ,
Differential expression patterns of Puma and Hsp70 following proteasomal stress in the hippocampus are key determinants of neuronal vulnerability
Authors: Helena P Bonner
Ina Woods
Caroline Bonner
Jochen H M Prehn
Manus W Ward
Caoimh√≠n G Concannon
Journal: Journal of Neurochemistry (2010)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Proteasomal stress; Ischemic brain injury; Neurodegenerative disorders; Organotypic hippocampal slice cultures (OHSCs); Proteasome inhibitors
Affiliations: Department of Physiology, Royal College of Surgeons in Ireland, Dublin, Ireland.

Abstract:  Proteasomal stress is believed to contribute to the pathology of ischemic brain injury and several neurodegenerative disorders, but can activate both cytoprotective and cell death-inducing pathways. Here we have utilized the complex environment of organotypic hippocampal slice cultures (OHSCs) to investigate the stress responses activated in different neuronal populations following proteasome inhibition. Incubation of OHSCs with the specific proteasome inhibitors, epoxomicin or bortezomib led to a selective injury of the CA1 pyramidal neurons although similarly increased levels of poly-ubiquitinylated proteins were detected throughout all regions of the hippocampus. Micro-dissection, quantitative PCR and immunohistochemical analyses of epoxomicin-treated OHSCs identified a selective activation of cytoprotective genes in non-vulnerable regions, and a selective activation of p53 target genes within the CA1. Genetic deletion of the pro-apoptotic p53 target gene, p53-upregulated modulator of apoptosis (puma), significantly reduced injury within the CA1 following proteasomal inhibition. Activation of cytoprotective genes by treatment with inducers of heat shock protein 70 inhibited the selective activation of p53 signaling within the CA1 and protected CA1 neurons from epoxomicin-induced cell death. In summary, we demonstrate that the reciprocal activation of p53/p53-upregulated modulator of apoptosis and heat shock protein 70 signalling determines the selective vulnerability of neurons to proteasome inhibition. 

Retracted: No

PubPeer comments:
 Figure 2(a). 24 h and 72 h panels much more similar to each other than either is to the 48 h panel. https: imgur.com 6bpzOx2 ,
Dual-targeted NIS polyplexes‚Äîa theranostic strategy toward tumors with heterogeneous receptor expression
Authors: Sarah Urnauer
Stephan Morys
Mariella Tutter
Kathrin A Schmohl
Christine Spitzweg
Sibylle Ziegler
Christina Schug
Ernst Wagner
Dirk-Andr√© Clevert
Peter Bartenstein
Nathalie Schwenk
Journal: Gene Therapy (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tumor heterogeneity; gene therapy; polymer-formulated nonviral vectors; dual-targeting approach; synthetic LPEI-PEG2kDa-based polymer
Affiliations: Department of Internal Medicine IV, University Hospital of Munich, LMU Munich, Germany., Department of Pharmacy, Center of Drug Research, Pharmaceutical Biotechnology, LMU Munich, Germany., Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Germany., Department of Clinical Radiology, University Hospital of Munich, LMU Munich, Germany., Department of Internal Medicine IV, University Hospital of Munich, LMU Munich, Germany. .

Abstract:  Tumor heterogeneity, within and between tumors, may have severe implications for tumor therapy, especially for targeted gene therapy, where single-targeted approaches often result in limited efficacy and therapy resistance. Polymer-formulated nonviral vectors provide a potent delivery platform for cancer therapy. To improve applicability for future clinical use in a broad range of patients and cancer types, a dual-targeting approach was performed. Synthetic LPEI-PEG2kDa-based polymer backbones were coupled to two tumor-specific peptide ligands GE11 (EGFR-targeting) and cMBP (cMET-targeting). The dual-targeting approach was used to deliver the theranostic sodium iodide symporter (NIS) gene to hepatocellular cancer. NIS as auspicious theranostic gene allows noninvasive imaging of functional NIS gene expression and effective anticancer radioiodide therapy. Enhanced tumor-specific transduction efficiency of dual-targeted polyplexes compared to single-targeted polyplexes was demonstrated in vitro using tumor cell lines with different EGFR and cMET expression and in vivo by 124I-PET-imaging. Therapeutic efficacy of the bispecific concept was mirrored by significantly reduced tumor growth and perfusion, which was associated with prolonged animal survival. In conclusion, the dual-targeting approach highlights the benefits of a bifunctional strategy for a future clinical translation of the bioimaging-based NIS-mediated radiotherapy allowing efficient targeting of heterogeneic tumors with variable receptor expression levels. 

Retracted: No

PubPeer comments:
 Figure 1: From my reading of this figure, it looks like a higher magnification image from one experimental condition is contained inside another panel, I ve added the magenta boxes to show where I mean. Was this intended? Could the authors please check?  ,
Culture of Methanogenic Archaea from Human Colostrum and Milk
Authors: Anthony Levasseur
Clotilde des Robert
V√©ronique Brevaut
Michel Drancourt
Ghiles Grine
Matthieu Million
Emeline Baptiste
Aurelia Caputo
Amadou Hamidou Togo
Didier Raoult
Marion Bonnet
Saber Khelaifia
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: Archaeal sequences; human colostrum; milk; living archaea; Methanogenic archaea
Affiliations: IHU-M√©diterran√©e Infection, Marseille, France., Aix Marseille Univ, IRD, APHM, MEPHI, Marseille, France., APHM, CHU H√¥pital de la Conception, Service de m√©decine n√©onatale, F-13385, Marseille, France., APHM, CHU H√¥pital Nord, Service de m√©decine n√©onatale, Marseille, France., IHU-M√©diterran√©e Infection, Marseille, France. ., Aix Marseille Univ, IRD, APHM, MEPHI, Marseille, France. .

Abstract:  Archaeal sequences have been detected in human colostrum and milk, but no studies have determined whether living archaea are present in either of these fluids. Methanogenic archaea are neglected since they are not detected by usual molecular and culture methods. By using improved DNA detection protocols and microbial culture techniques associated with antioxidants previously developed in our center, we investigated the presence of methanogenic archaea using culture and specific Methanobrevibacter smithii and Methanobrevibacter oralis real-time PCR in human colostrum and milk. M. smithii was isolated from 3 colostrum and 5 milk (day 10) samples. M. oralis was isolated from 1 milk sample. For 2 strains, the genome was sequenced, and the rhizome was similar to that of strains previously isolated from the human mouth and gut. M. smithii was detected in the colostrum or milk of 5/13 (38%) and 37/127 (29%) mothers by culture and qPCR, respectively. The different distribution of maternal body mass index according to the detection of M. smithii suggested an association with maternal metabolic phenotype. M. oralis was not detected by molecular methods. Our results suggest that breastfeeding may contribute to the vertical transmission of these microorganisms and may be essential to seed the infant's microbiota with these neglected critical commensals from the first hour of life. 

Retracted: No

PubPeer comments:
 Let $$alpha=(0, 1, 0)$$ $$beta=(0, 0, 1)$$ It follows from Definition 3 that $$alpha otimes beta = (0, 1, 1)$$ which **is not a picture fuzzy number in the sense of Definition 1**. A theory based on such notions, like the methods presented in this paper, make no sense. See also https: pubpeer.com publications 6714C6C2D8100E026807E2746B0B4B https: pubpeer.com publications FAE24E6C38326C60F3EE601F6D0C1A   , 
 A part of the reference list is attached. 46 out of the total 83 cited papers are authored by G.W. Wei and his co-authors.   ,
Perilipin 5 Deletion in Hepatocytes Remodels Lipid Metabolism and Causes Hepatic Insulin Resistance in Mice
Authors: Jennifer C Y Lo
Stacey N Keenan
Andrew Ryan
Matthew J Watt
Magdalene K Montgomery
Ruth C Meex
Shuai Nie
Journal: Diabetes (2019)
Discipline: CLINICAL MEDICINE
Keywords: hepatic lipid metabolism; nonalcoholic fatty liver disease; insulin resistance; lipid droplet metabolism; perilipin 5
Affiliations: Metabolism, Diabetes and Obesity Program, Monash Biomedicine Discovery Institute, and Department of Physiology, Monash University, Clayton, Victoria, Australia., Department of Human Biology, School of Nutrition and Translational Research in Metabolism (NUTRIM), Faculty of Health, Medicine and Life Sciences, Maastricht University Medical Centre, Maastricht, the Netherlands., TissuPath, Mount Waverley, Victoria, Australia., Melbourne Mass Spectrometry and Proteomics Facility, Bio21 Molecular Science & Biotechnology Institute, The University of Melbourne, Melbourne, Victoria, Australia., Department of Physiology, The University of Melbourne, Melbourne, Victoria, Australia., Metabolism, Diabetes and Obesity Program, Monash Biomedicine Discovery Institute, and Department of Physiology, Monash University, Clayton, Victoria, Australia .

Abstract:  Defects in hepatic lipid metabolism cause nonalcoholic fatty liver disease and insulin resistance, and these pathologies are closely linked. Regulation of lipid droplet metabolism is central to the control of intracellular fatty acid fluxes, and perilipin 5 (PLIN5) is important in this process. We examined the role of PLIN5 on hepatic lipid metabolism and systemic glycemic control using liver-specific Plin5-deficient mice (Plin5LKO ). Hepatocytes isolated from Plin5LKO mice exhibited marked changes in lipid metabolism characterized by decreased fatty acid uptake and storage, decreased fatty acid oxidation that was associated with reduced contact between lipid droplets and mitochondria, and reduced triglyceride secretion. With consumption of a high-fat diet, Plin5LKO mice accumulated intrahepatic triglyceride, without significant changes in inflammation, ceramide or diglyceride contents, endoplasmic reticulum stress, or autophagy. Instead, livers of Plin5LKO mice exhibited activation of c-Jun N-terminal kinase, impaired insulin signal transduction, and insulin resistance, which impaired systemic insulin action and glycemic control. Re-expression of Plin5 in the livers of Plin5LKO mice reversed these effects. Together, we show that Plin5 is an important modulator of intrahepatic lipid metabolism and suggest that the increased Plin5 expression that occurs with overnutrition may play an important role in preventing hepatic insulin resistance. 

Retracted: No

PubPeer comments:
 How can you measure Lipogenesis using 2-3H glucose when it loses its label in upper glycolysis in the hydrogen exchanges at phosphoglucose isomerase? ,
Synthesis of a well-dispersed CaFe2O4/g-C3N4/CNT composite towards the degradation of toxic water pollutants under visible light
Authors: Zhaoxiang Zhang
Fei Liu
Zheng Zheng
Kun Liu
Xiaqing Li
Yanping Xin
Shaocan Dong
Xiaodong Dai
Zhenhe Yuan
Xuewu Wang
Journal: RSC Advances (2019)
Discipline: CHEMISTRY
Keywords: ternary photocatalyst; CaFe2O4; multiwalled carbon nanotubes; CNT; graphitic carbon nitride
Affiliations: Shengli College, China University of Petroleum, Dongying, China, Shengli Oilfield Company Postdoctoral Research Station, Sinopec, Petroleum Engineering Technology Research Institute of Shengli Oilfield Company, SINOPEC

Abstract:  Herein, we fabricated a ternary photocatalyst composed of CaFe2O4, multiwalled carbon nanotubes (CNTs) and graphitic carbon nitride (g-C3N4) via a simple hydrothermal route. CaFe2O4 acted as a photosensitizer medium and the CNT acted as a co-catalyst, which remarkably enhanced the photocatalytic performances of g-C3N4 towards the degradation of hexavalent chromium (Cr(vi)) and the antibiotic tetracycline (TC) under visible light irradiation. To investigate the morphological and topological features of the photocatalyst, field-emission scanning electron microscopy (FE-SEM) and transmission electron microscopy (TEM) analyses were performed. The surface properties and oxidation state of the CaFe2O4/g-C3N4/CNT composite were determined by X-ray photoelectron spectroscopy (XPS). The recombination rate of the charge carriers and the band gap values of the as-synthesized catalysts were analyzed by photoluminescence spectroscopy (PL) and diffused reflectance spectroscopy (UV/Vis DRS) studies, respectively. Besides the degradation reactions, the high hydrogen production rate of 1050 Œºmol h-1 under visible light using the CaFe2O4/g-C3N4/CNT composite loaded with 5 wt% CNT was observed. The superior photocatalytic performances of the CaFe2O4/g-C3N4/CNT composite can be ascribed to the effective heterojunction formed between g-C3N4 and the CaFe2O4 matrix, in which the CNT act as a conducting bridge in the system, promoting the production of photoinduced charge carriers in the semiconductor system. Finally, the plausible photocatalytic mechanism towards the degradation of pollutants and hydrogen production was discussed carefully. 

Retracted: No

PubPeer comments:
 Figure 2 panel A and Figure 3 panel A beta-actin western blot signal looks remarkably similar however should represent different experiments: adipose tissue vs. visceral adipose tissue. Figure 2A:  Figure 3A:  Compare:  ,
Downregulating circRNA_0044516 Inhibits Cell Proliferation in Gastric Cancer Through miR-149/Wnt1/Œ≤-catenin Pathway
Authors: Xiangling Meng
Jun Fang
Wei Chen
Journal: Journal of Gastrointestinal Surgery (2020)
Discipline: CLINICAL MEDICINE
Keywords: Cell proliferation; CircRNA_0044516; Gastric cancer; Wnt1; miR-149.
Affiliations: Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, NO. 218 Jixi Rd, Hefei, 230022, Anhui Province, China. ., Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, NO. 218 Jixi Rd, Hefei, 230022, Anhui Province, China.

Abstract:  Background: Circular RNAs (circRNAs) play important roles in the progression of gastric cancer (GC). The Wnt1/Œ≤-catenin pathway can promote the proliferation of GC cells. This study aimed to explore whether circRNA_0044516 can regulate the proliferation of GC cells by modulating the Wnt1/Œ≤-catenin pathway. Methods: The expression of circRNA_0044516, miR-149, Wnt1, and Œ≤-catenin in GC tissues or cells was detected by qRT-PCR and western blot. Cell viability and apoptosis were measured by CCK-8 and flow cytometry assays, respectively. The interaction between circRNA_0044516 and miR-149 was determined by luciferase reporter and RNA pull-down assays. Results: Upregulated circRNA_0044516 was found in GC tissues and cell lines. Downregulating circRNA_0044516 inhibited the viability and promoted apoptosis of GC cells. CircRNA_0044516 targeted miR-149, and its downregulation elevated miR-149 level in GC cells. Mechanistically, silencing circRNA_0044516 reduced the protein level of Wnt1 and Œ≤-catenin through miR-149, and finally suppressed viability and contributed to apoptosis of GC cells. Moreover, circRNA_0044516 knockdown inhibited the tumor growth of HGC-27 cells in nude mice. Conclusions: Our results indicated an important role of circRNA_0044516 in GC and elucidated that downregulation of circRNA_0044516 inhibits the proliferation of GC cells through miR-149/Wnt1/Œ≤-catenin. 

Retracted: No

PubPeer comments:
 Fig. 5 A and 5 C are more similar than expected. Can the authors please check?  ,