PReD-Bench/PRed-Bench huggingface dataset:
Oleaginous yeasts from Ethiopia
Authors: Carolina Pohl
Nicholas Kiggundu
Marizeth Groenewald
Dawit Abate
Tamene Milkessa Jiru
Journal: AMB Express (2016)
Discipline: MICROBIOLOGY
Keywords: Biodiesel; Oleaginous yeast; Single cell oil; Yeast identification.
Affiliations: Microbial, Cellular and Molecular Biology Department, College of Natural Sciences, Addis Ababa University, P.O. Box: 1176, Addis Ababa, Ethiopia. ., Microbial, Cellular and Molecular Biology Department, College of Natural Sciences, Addis Ababa University, P.O. Box: 1176, Addis Ababa, Ethiopia., Department of Agricultural and Biosystems-Engineering, School of Food Technology, Nutrition and Bio-Engineering, Makerere University, P.O. Box: 7062, Kampala, Uganda., Department of Microbial, Biochemical and Food Biotechnology, College of Agricultural Sciences, University of the Free State, P.O. Box: 339, Bloemfontein, South Africa., CBS-KNAW Fungal Biodiversity Center, Uppsalalaan 8, P.O. Box: 85167, 3584 CT, Utrecht, The Netherlands.

Abstract:  Oleaginous microorganisms can produce high amounts of oil (&gt;20 % of their biomass) under suitable cultivation conditions. In this research work 200 samples were collected from soil, plant surfaces (leaves, flowers and fruits), waste oils from traditional oil milling houses and dairy products (cheese, milk and yoghurt) in Ethiopia. Three hundred and forty yeast colonies were isolated from these samples. By applying Sudan III staining tests, 18 strains were selected as possible oleaginous yeasts. The 18 strains were identified and characterized for their lipid production as a feedstock for biodiesel production in the future. They were identified using morphological and physiological methods as well as sequencing the 3'end of the small-subunit rRNA gene, the internal transcribed spacer regions (ITS; ITS 1, ITS 2 and the intervening 5.8S rRNA gene), and the D1/D2 domain of the 26S rRNA gene. The 18 yeasts were identified as Cutaneotrichosporon curvatus (syn, Cryptococcus curvatus) (PY39), Rhodotorula kratochvilovae (syn, Rhodosporidium kratochvilovae) (SY89), Rhodotorula dairenensis (SY94) and Rhodotourula mucilaginosa (SY09, SY18, SY20, PY21, PY23, PY25, SY30, PY32, SY43, PY44, SY52, PY55, PY61, SY75 and PY86). Under nitrogen-limited cultivation conditions, R. mucilaginosa PY44 produced the highest biomass (15.10 ¬± 0.54 g/L), while R. mucilaginosa PY32 produced the lowest biomass (10.32 ¬± 0.18 g/L). The highest lipid yield of 6.87 ¬± 0.62 g/L and lipid content of 46.51 ¬± 0.70 % were attained by C. curvatus (syn, C. curvatus) PY39. On the other hand, R. mucilaginosa PY61 gave the lowest lipid yield (2.06 ¬± 0.52 g/L) and R. mucilaginosa SY52 gave the lowest lipid content of 16.99 ¬± 0.85 %. The results in this research work suggest that much more oleaginous yeasts can be isolated from Ethiopian environment. On the basis of their substantial lipid production abilities, the three oleaginous yeast strains PY39, SY89 and SY18 were selected and recommended for further optimization processes. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have 2 images which overlap, although described as representing different yeast strains. ***  ,
Synthesis and Characterization of Natural Nano-hydroxyapatite Derived from Turkey Femur-Bone Waste
Authors: Mohammad Irani
Amirhossein Esmaeilkhanian
Fariborz Sharifianjazi
Aliasghar Abouchenari
Nader Parvin
Amirreza Rouhani
Journal: Applied Biochemistry and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Ball mill; Nano-hydroxyapatite; Sintering; Turkey femur-bone waste.
Affiliations: Mining and Metallurgical Engineering Department, Amirkabir University of Technology, Tehran, Iran., Mining and Metallurgical Engineering Department, Amirkabir University of Technology, Tehran, Iran. ., Department of Material Science and Engineering, Shahid Bahonar University of Kerman, Kerman, 7618868366, Iran., Department of Mechanical, Industrial & Aerospace Engineering, Concordia University, Montreal, Canada., Department of Chemical Engineering, Amirkabir University of Technology, Tehran, Iran.

Abstract:  Hydroxyapatite (HAp) is a bioactive and vital material which has found many applications in the biomedical and clinical fields. This bio-ceramic powder can be synthesized via different bio-waste materials. In this study, the production of natural nanohydroxyapatite was produced through calcination of untreated turkey femur-bone waste powder at 850 ¬∞C followed by ball milling the powder. The obtained powder was characterized using X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR) analysis. The morphology, size, and elemental composition of obtained turkey hydroxyapatite (THA) particles were investigated by scanning electron microcopy (SEM), transmission electron microcopy (TEM), and energy dispersive spectroscopy (EDS) analysis, in which the average particle size of ball milled THA was found to be about 85 nm with a Ca/P ratio of 1.63. The powder was then cold pressed and later sintered at 850, 950, 1050, and 1150 ¬∞C to evaluate its mechanical properties in terms of compressive strength and hardness. The results revealed that the strength and hardness of the samples increased by increasing the sintering temperature up to 1150 ¬∞C. Finally, the maximum values of hardness and compressive strength of the sintered THA were obtained at 1150 ¬∞C (37.44 MPa and 3.2 GPa, respectively). 

Retracted: No

PubPeer comments:
 Fig. 1 XRD pattern of THA powder after ball mill process Four identical XRD patterns presented as 4 different samples  ,
A dual functional ruthenium arene complex induces differentiation and apoptosis of acute promyelocytic leukemia cells
Authors: Yaqiong Kong
Siming Yuan
Yangzhong Liu
Kaiming Cao
Hai Huang
Hongke Liu
Yucai Wang
Journal: Chemical Science (2019)
Discipline: CHEMISTRY
Keywords: acute promyelocytic leukemia; PML; RARŒ± genes; Ru(ii) arene complex; zinc-release
Affiliations: CAS Key Laboratory of Soft Matter Chemistry , Department of Chemistry , University of Science and Technology of China , Hefei , Anhui 230026 , China . Email: ., Jiangsu Key Laboratory of Biofunctional Materials , College of Chemistry and Materials Science , Nanjing Normal University , Nanjing , Jiang Su 210046 , China., School of Life Sciences and Medical Center , University of Science and Technology of China , Hefei , Anhui 230027 , China.

Abstract:  Human acute promyelocytic leukemia (APL) is the most malignant form of acute leukemia. The fusion of PML and RARŒ± genes is responsible for over 98% of cases of APL. In this work, we found that a Ru(ii) arene complex, [(Œ∑6-p-bip)Ru(en)Cl][PF6] (Ru-1), can selectively react with PML, leading to zinc-release and protein unfolding. Consequently, the degradation of the fusion protein PML-RARŒ± occurs, which causes the differentiation of APL cells. In addition, Ru-1 can also bind to DNA and trigger apoptosis of APL cells. Therefore, Ru-1 acts as a dual functional agent that inhibits the growth of APL cells and induces cell differentiation. In contrast, the other non-selective Ru(ii) compound, though also highly reactive to PML, does not exhibit anti-APL activity. The selectivity of Ru-1 to PML suggests a new strategy for the development of anti-APL drugs using ruthenium agents. 

Retracted: No

PubPeer comments:
 Strange PARP cleaved PARP and caspase 3 cleaved caspase 3 blots for an apoptosis-inducing compound.  Figure 6a. In text: u201cThe alteration of the levels of these proteins occurred in a time dependent manner, and significant changes occurred after the drug treatment for 4u20138 h.u201d which has no semblance to the figure, either. No accusation of manipulation at all here but these blots are almost certainly upside down and I suspect have been assigned incorrectly. See below for my edit, which is a 180 rotation and would show PARP caspase 3 cleavage at 20 hrs, as you d expect for an apoptosis-inducing compound (which they have used at far greater levels than the IC50 concentration to show this outcome). My edit:  ,
Knockdown of GRP78 enhances cell death by cisplatin and radiotherapy in nasopharyngeal cells
Authors: Long-Jian Pu
Hao Liu
Ying-Ying Huang
Lin-Yan Ma
Chen-Chen Jiang
Le-Le Song
Journal: Anti-Cancer Drugs (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Radiotherapy; adjuvant cisplatin chemotherapy; nasopharyngeal carcinoma; treatment strategies; endoplasmic reticulum stress
Affiliations: aDepartment of Pharmacy, the First Affiliated Hospital of Bengbu Medical College bBengbu Medical College, Faculty of Pharmacy, Bengbu, Anhui, People's Republic of China cSchool of Medicine and Public Health, The University of Newcastle, Newcastle, New South Wales, Australia.

Abstract:  Radiotherapy and adjuvant cisplatin chemotherapy are the mainstream approaches in the treatment of nasopharyngeal carcinoma (NPC). These have been shown to effectively improve the outcome and reduce tumor recurrence. However, radiotherapy and chemotherapy resistance during the course of treatment has become more common recently, resulting in the failure of NPC therapy. Therefore, new therapeutic strategies or adjuvant drugs are urgently needed. The current study was designed to look for new treatment strategies or auxiliary drugs in the treatment of NPC. Two human NPC cell lines, HNE1 and HNE1/DDP, were used to examine the relationship between endoplasmic reticulum stress and cell resistance to ionizing radiation (IR) and cisplatin (DDP). Cell proliferation was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Meanwhile, propidium iodide (PI) staining and PI/Annexin V staining were used to observe cell apoptosis. Finally, western blot was used to detect the endogenous expression of glucose-regulated protein 78 (GRP78) and other apoptosis-related proteins. GRP78 small interference RNA was transfected using Lipofectamine 2000. Compared with HNE1/DDP, IR and DDP increased the cell apoptosis and inhibited the cell proliferation of HNE1. Inhibition of GRP78 can reverse IR and DDP resistance in NPC cells by PI/Annexin V staining. Knockdown of GRP78 upregulates the expression of pro-apoptotic proteins and downregulates the expression of antiapoptotic proteins. These results indicate that HNE1 is more sensitive to DDP and IR than HNE1/DDP. Knockdown GRP78 can reverse IR and DDP resistance in NPC cells. Inhibition of GRP78 gives us a new target to overcome resistance to radiotherapy and chemotherapy of NPC cells. Thus, this study should be further explored in vivo and assessed for possible clinical applications. 

Retracted: No

PubPeer comments:
 Fig. 3a and Fig. 3b. More similar than expected, with the different exposure of the WB bands.  , 
 Fig. 3a and Fig. 4a. More similar than expected.  ,
The enhancement of neural stem cell survival and growth by coculturing with expanded Sertoli cells in vitro
Authors: Jingxiu Bi
Xiaolin Shi
Meijin Guo
Lei Deng
Bingyang Shi
Hu Zhang
Yonghong Wang
Sheng Dai
Journal: Biotechnology Progress (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Sertoli cells; culture conditions; neural stem cells; metabolic activity; secreted proteins
Affiliations: State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, PR China.

Abstract:  Sertoli cells (SCs) have been described as the "nurse cells" of testis to provide essential growth factors and to create a proper environment for the development of other cells (e.g., germinal and neural stem cell). However, the physiological functions of the SCs obtained from different culture conditions are different in a coculturing system, and thus the optimal SC culturing condition should be investigated in vitro. In this paper, primary Sertoli cells were isolated from a 12-day-old mouse and expanded in two different culture conditions: a two dimensional (2D) plastic tissue disc and a three dimensional (3D) microcarrier culture system. They were then cocultured with neural stem cells (NSCs) isolated from 14-day-old mouse embryos. The metabolic activities of SCs(2D) (SCs in 2D) and SCs(3D) (SCs in 3D) and the amount of proteins secreted from two culturing systems were compared. The results show that the metabolic activity and the amount of secreted proteins from SCs(3D) were higher than both from SCs(2D). Three coculturing groups: NSCs+SC(2D), NSCs+SC(3D), and NSCs +SC-conditioned medium (SCCM, control group) were also compared regarding cell morphology and the numbers of neurons, neural outgrowths and neurospheres. The quantity of neurons, neural outgrowths and neurospheres were the highest in the NSCs+SC(3D) group. SCs cultured in the 3D system had a strong trophic effect on NSCs and enhanced their survival and growth. Besides, the mRNA of trophic and nutritive factors such as Glial-cell-line-derived neurotrophic factor (GDNF) and Interleukin-1 Œ± (IL-1 Œ±) secreted by the SCs from both 2D and 3D culture system were analyzed by real time-PCR and gel assay. The mRNA transcription of GDNF and IL-1Œ± is more apparent in the 3D culture system than that from the 2D one. The coculturing system of NSCs+SC(3D) is a promising candidate for future neural stem cell transplantation. 

Retracted: No

PubPeer comments:
 Figure 6. * Yellow boxes: Two panels representing different treatments and timepoints appear to look very similar, although the red arrows are positioned at different locations.  , 
 Correction, September 2021, found here: https: aiche.onlinelibrary.wiley.com doi 10.1002 btpr.3199  The authors regret that an inadvertent error (Figure H was the same as Figure C) was observed in Figure 6. The corrected Figure 6H are now incorporated in Figure 6. This correction does not influence any of the experimental results and discussion or the conclusions reported in the paper. The authors sincerely apologize to the editors and readers for any inconvenience. I thank the authors and editors for correcting this error. ,
Agonism of GPR120 prevents ox-LDL-induced attachment of monocytes to endothelial cells
Authors: Long Liu
Lirong Zhang
Tiechao Jiang
Dong You
Qini Zhao
Dongli Jiang
Journal: Chemico-Biological Interactions (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Atherosclerosis; E-selectin; GPR120; HAECs; KLF2
Affiliations: Department of Cardiovascular Medicine, China-Japan Union Hospital of Jilin University, Changchun, 130033, China; Jilin Provincial Precision Medicine Key Laboratory for Cardiovascular Genetic Diagnosis, 130033, China., Department of Pharmacy, China-Japan Union Hospital of Jilin University, Changchun, 130033, China., Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, 130021, China., Department of Pathology, China-Japan Union Hospital of Jilin University, Changchun, 130033, China., Department of Cardiovascular Medicine, China-Japan Union Hospital of Jilin University, Changchun, 130033, China; Jilin Provincial Precision Medicine Key Laboratory for Cardiovascular Genetic Diagnosis, 130033, China. Electronic address: .

Abstract:  Oxidized low-density lipoprotein (ox-LDL)-induced endothelial inflammation plays an important role in the development of cardiovascular diseases. G protein-coupled receptors (GPCR) are gaining traction as potential treatment targets due to their roles in mediating a wide range of physiological processes. GPR120 is a recently identified omega-3 fatty acid receptor. We hypothesized that agonism of GPR120 might attenuate ox-LDL-induced endothelial dysfunction. In the present study, we tested the effects of two GPR120 agonists-GW9508 and TUG-891-in mitigating endothelial insult induced by ox-LDL in human aortic endothelial cells (HAECs). Real-time PCR, western blot, and ELISA analyses were used in our experiments. Our findings demonstrate that GPR120 is downregulated by exposure to ox-LDL, suggesting a role for GPR120 in mediating ox-LDL insult. Furthermore, we found that agonism of GPR120 could suppress oxidative stress and inflammation by inhibiting the production of reactive oxygen species and the expression of proinflammatory cytokines. Importantly, we show that agonism of GPR120 prevents the attachment of monocytes to endothelial cells by suppressing the expression of VCAM-1 and E-selectin. Finally, we show that agonism of GPR120 exerts a remarkable atheroprotective effect by elevating the expression level of Kr√ºppel-like factor 2 (KLF2). Together, our results demonstrate a potential role for specific agonism of GPR120 in the prevention of endothelial damages induced by ox-LDL. 

Retracted: No

PubPeer comments:
 When exposure is adjusted several areas of sharp contrast appear in the images of Figure 7. Could the authors check the original images? *** Adjusted  *** Unadjusted  ,
Protocatechuic aldehyde mitigates hydrogen peroxide-triggered PC12¬†cell damage by down-regulating MEG3
Authors: Xiaoyuan Yao
Zhiwei Zhong
Lina Dong
Rui Jiang
Min Luo
Ziyan Zhang
Mei Li
Journal: Artificial Cells Nanomedicine and Biotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PTEN/PI3K/AKT; Spinal cord injury; Wnt/Œ≤-catenin; hydrogen peroxide; protocatechuic aldehyde.
Affiliations: Department of Pain, China-Japan Union Hospital of Jilin University, Jilin, China, Department of Pathology, Changchun Medical College, Jilin, China, Department of Medical Insurance Management, China-Japan Union Hospital of Jilin University, Jilin, China, Department of Orthopedics, The Second Hospital of Jilin University, Jilin, China, Department of Orthopedics, China-Japan Union Hospital of Jilin University, Jilin, China

Abstract:  Background: Protocatechuic aldehyde (PA) extracts from S. miltiorrhiza, which anti-oxidative and anti-inflammatory functions have been certified in diverse diseases. Nonetheless, the influence of PA in spinal cord injury (SCI) is still hazy. The research probed the function of PA in hydrogen peroxide (H2O2)-damaged PC12 cells.Methods: The disparate dosages of H2O2 (0-400 ¬µM) or PA (0-2 ¬µM) were applied for stimulating PC12 cells, and subsequently cell viability, apoptosis, apoptosis- and autophagy-correlative factors were evaluated. After pc-MEG3 transfection, functions of MEG3 overexpression in H2O2 and/or PA-managed PC12 cells were reassessed. Western blot was conducted to determine Wnt/Œ≤-catenin and PTEN/PI3K/AKT pathways.Results: H2O2 stimulation clearly triggered PC12 cell damage via prohibiting cell viability and accelerating apoptosis and autophagy. But, PA management mitigated H2O2-triggered PC12 cells damage. Down-regulated MEG3 triggered by PA was presented in H2O2-managed cells. What's more, overexpressed MEG3 dramatically overturned the influences of PA in H2O2-damaged PC12 cells. Beyond that, PA activated Wnt/Œ≤-catenin and PTEN/PI3K/AKT via repression of MEG3 in H2O2-managed PC12 cells.Conclusions: The results disclosed the protective impacts of PA on PC12 cells to resist H2O2-provoked damage. MEG3, Wnt/Œ≤-catenin and PTEN/PI3K/AKT pathways joined in adjusting the activity of PA in H2O2-damaged PC12 cells. 

Retracted: No

PubPeer comments:
 All the Western Blots in this paper have a curious stylised appearance, with the bands retaining a constant flat profile and the same general appearance for all the proteins of interest. The protein blobs seem to come from the same universe as the tadpoles or performing sardines familiar from the products of the celebrated  Tadpole Papermill . Here, Fig 6A C.  Is it possible for the authors to upload scans of the original gels? ,
<em>miR-218</em> overexpression suppresses tumorigenesis of papillary thyroid cancer via inactivation of PTEN /PI3K/AKT pathway by targeting Runx2
Authors: Liwei Chen
Mingkun Han
Yang Wang
Journal: OncoTargets and Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: PTEN/PI3K/AKT; Runx2; miR-218; papillary thyroid cancer.
Affiliations: Department of Otolaryngology Head and Neck Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China, .

Abstract:  Background: It was previously reported that downregulation of miR-218 promoted thyroid cancer cell invasion, migration, and proliferation. However, the biological functions of miR-218 and its possible regulatory mechanisms in papillary thyroid cancer (PTC) cells are still elusive. Materials and methods: The expression levels of miR-218 and Runx2 in PTC tissues and cells were determined by quantitative real-time PCR (qRT-PCR) and Western blot. The effects of miR-218 overexpression on cell viability, invasion, apoptosis, and PTEN/PI3K/AKT pathway in PTC cells were evaluated by cell counting kit-8 assay, Transwell invasion assay, flow cytometry assay, and Western blot, respectively. Luciferase reporter assay and qRT-PCR were performed to identify the target of miR-218. Xenograft tumor experiment was performed to confirm the biological roles of miR-218 and its potential mechanisms in vivo. Results: miR-218 expression was downregulated and Runx2 expression was upregulated in PTC tissues and cells. Overexpression of miR-218 suppressed viability and invasion, and induced apoptosis of PTC cells in vitro, while Runx2 overexpression greatly abolished these effects. miR-218 overexpression inactivated the PTEN/PI3K/AKT pathway, which was abated by Runx2 upregulation. Additionally, Runx2 was validated to be a direct target of miR-218. Moreover, enforced expression of miR-218 inhibited tumor growth and Runx2 expression, and blocked PTEN/PI3K/AKT pathway in vivo. Conclusion: miR-218 overexpression suppresses the tumorigenesis of PTC via downregulating PTEN/PI3K/AKT pathway by targeting Runx2, which indicates that miR-218 may be a potential therapeutic target for human PTC. 

Retracted: No

PubPeer comments:
 Fig 3.  Effects of miR-218 overexpression on tumorigenesis of PTC in vitro. Notes: K-1 and TPC-1 cells were transfected with miR-218 or miR-control, and further experiments were performed at 24 or 48 hours post-transfection.... Cell invasive ability was examined by Transwell invasion assay in transfected (C) K-1 and (D) TPC-1 cells. Internal duplications marked.  ,
Para-aminobenzoic acid (PABA) synthase enhances thermotolerance of mushroom Agaricus bisporus
Authors: Yuemao Shen
Meiyuan Chen
Zhonglei Lu
Liang Zhu
Siyang Song
Xiangxiang Kong
Zhaoming Lu
Xiangyang Hu
Meixiang Xiao
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: mushrooms; thermotolerance; proteomic; heat stress; proteins
Affiliations: State Key Laboratory of Stress Cell Biology, School of Life Science, Xiamen University, Xiamen, Fujian, China., Key Laboratory of Biodiversity and Biogeography, Kunming Institute of Botany, Institute of Tibet Plateau Research at Kunming, Chinese Academy of Science, Kunming, Yunnan, China., Edible Fungi Institute of Fujian Academy of Agricultural Sciences. Fuzhou, Fujian, China., Department of Developmental and Molecular Biology, and Medicine, Albert Einstein College of Medicine, Bronx, NY, United States of America.

Abstract:  Most mushrooms are thermo-sensitive to temperatures over 23¬∞C, which greatly restricts their agricultural cultivation. Understanding mushroom's innate heat-tolerance mechanisms may facilitate genetic improvements of their thermotolerance. Agaricus bisporus strain 02 is a relatively thermotolerant mushroom strain, while strain 8213 is quite thermo-sensitive. Here, we compared their responses at proteomic level to heat treatment at 33¬∞C. We identified 73 proteins that are differentially expressed between 02 and 8213 or induced upon heat stress in strain 02 itself, 48 of which with a known identity. Among them, 4 proteins are constitutively more highly expressed in 02 than 8213; and they can be further upregulated in response to heat stress in 02, but not in 8213. One protein is encoded by the para-aminobenzoic acid (PABA) synthase gene Pabs, which has been shown to scavenge the reactive oxygen species in vitro. Pabs mRNA and its chemical product PABA show similar heat stress induction pattern as PABA synthase protein and are more abundant in 02, indicating transcriptional level upregulation of Pabs upon heat stress. A specific inhibitor of PABA synthesis impaired thermotolerance of 02, while exogenous PABA or transgenic overexpression of 02 derived PABA synthase enhanced thermotolerance of 8213. Furthermore, compared to 8213, 02 accumulated less H2O2 but more defense-related proteins (e.g., HSPs and Chitinase) under heat stress. Together, these results demonstrate a role of PABA in enhancing mushroom thermotolerance by removing H2O2 and elevating defense-related proteins. 

Retracted: No

PubPeer comments:
 Figure 5A. * Blue boxes: In the 02 panels, 23C column, the  vehicle and  PABA panels look very similar if one of them is rotated 180 degrees.  , 
 * you miss 33 degrees with 5 mg PABA - this is actually a blue triplicate (but moved slightly to the left) , 
 Thank you Hamopontonia, for your additional find. Here is a new illustration:  ,
Activation of NF-kappaB by alloferon through down-regulation of antioxidant proteins and IkappaBalpha
Authors: Myung-Jeom Ryu
Cheolju Lee
Hyesung Jeon
Seok-Ho Hong
Yeon Gyu Yu
Myeong-Hee Yu
Sergey Chernysh
Vadim Anikin
Journal: Molecular and Cellular Biochemistry (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Alloferon; NK cytotoxic activity; interferon synthesis; antiviral activity; antitumor activity
Affiliations: Life Sciences Division, Korea Institute of Science and Technology, 39-1 Hawolgok, Seongbuk, Seoul 136-791, Korea.

Abstract:  Alloferon is a 13-amino acid peptide isolated from the bacteria-challenged larvae of the blow fly Calliphora vicina. The pharmaceutical value of the peptide has been well demonstrated by its capacity to stimulate NK cytotoxic activity and interferon (IFN) synthesis in animal and human models, as well as to enhance antiviral and antitumor activities in mice. Antiviral and the immunomodulatory effectiveness of alloferon have also been supported clinically proved in patients suffering with herpes simplex virus (HSV) and human papilloma virus (HPV) infections. To elucidate molecular response to alloferon treatment, we initially screened a model cell line in which alloferon enhanced IFN synthesis upon viral infection. Among the cell lines tested, Namalva was chosen for further proteomic analysis. Fluorescence difference gel electrophoresis (DIGE) revealed that the levels of a series of antioxidant proteins decreased after alloferon treatment, while at least three glycolytic enzymes and four heat-shock proteins were increased in their expression levels. Based on the result of our proteomic analysis, we speculated that alloferon may activate the NF-kappaB signaling pathway. IkappaB kinase (IKK) assay, Western blot analysis on IkappaBalpha and its phosphorylated form at Ser 32, and an NF-kappaB reporter assay verified our proteomics-driven hypothesis. Thus, our results suggest that alloferon potentiates immune cells by activating the NF-kappaB signaling pathway through regulation of redox potential. Since NF-kappaB activation is involved in IFN synthesis, our results provide further clues as to how the alloferon peptide may stimulate IFN synthesis. 

Retracted: No

PubPeer comments:
 Figure 3. * Red boxes: two b-tubulin panels belonging to different experiments appear to look similar to each other. Reported to the journal in October 2015, but nothing has been done as of today.  ,
Early anticoagulation therapy for severe burns complicated by inhalation injury in a rabbit model
Authors: Guang-Hua Guo
Jinhua Luo
Ming-Zhuo Liu
Zhen-Fang Xiong
Xincheng Liao
Zhong-Hua Fu
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: early anticoagulation treatment; severe burns; inhalation injury; rabbit model; lung injury
Affiliations: Department of Burns, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China., Department of Pathology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Abstract:  The aim of the present study was to determine the effects of early anticoagulation treatment on severe burns complicated by inhalation injury in a rabbit model. Under anesthetization, an electrical burns instrument (100ÀöC) was used to scald the backs of rabbits for 15 sec, which established a 30% III severe burns model. Treatment of the rabbits with early anticoagulation effectively improved the severe burns complicated by inhalation injury‚Äëinduced lung injury, reduced PaO2, PaCO2 and SPO2 levels, suppressed the expression of tumor necrosis factor‚ÄëŒ? interleukin (IL)‚Ä?Œ≤ and IL‚Ä?, and increased the activity of IL‚Ä?0. In addition, it was found that early anticoagulation treatment effectively suppressed the activities of caspase‚Ä? and caspase‚Ä?, upregulated the protein expression of vascular endothelial growth factor (VEGF) and decreased the protein expression of protease‚Äëactivated receptor 1 (PAR1) in the severe burns model. It was concluded that early anticoagulation treatment affected the severe burns complicated by inhalation injury in a rabbit model through the upregulation of VEGF and downregulation of PAR1 signaling pathways. Thus, early anticoagulation is a potential therapeutic option for severe burns complicated by inhalation injury. 

Retracted: No

PubPeer comments:
 Figure 1. * Blue boxes: The Sham and Union panels appear to show an area of overlap, with a very different zoom factor * Red boxes: The Model and Antithrombin panels appear to show an area of overlap, with a very different zoom factor  ,
Hispidulin induces mitochondrial apoptosis in acute myeloid leukemia cells by targeting extracellular matrix metalloproteinase inducer
Authors: Jianjun Peng
Hui Gao
Yongji Liu
Tianhui Wu
Kan Li
Fanbo Jing
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Akt; EMMPRIN; Hispidulin; STAT3; apoptosis.
Affiliations: Qingdao University Medical College Qingdao, Shandong, 266071, China., Qingdao Hiser Medical Center Qingdao, Shandong 266000, China., Shandong Provincial Hospital Affiliated to Shandong University Shandong 250021, China., Qingdao 5th People's Hospital Qingdao, Shandong 266000, China., College of Life Sciences, Chongqing Normal University Chongqing 401331, China., The Affiliated Hospital of Qingdao University Qingdao, Shandong 266003, China.

Abstract:  Acute myeloid leukemia (AML) represents a heterogeneous group of hematological neoplasms with marked heterogeneity in response to both standard therapy and survival. Hispidulin, a flavonoid compound that is anactive ingredient in the traditional Chinese medicinal herb Salvia plebeia R. Br, has recently been reported to have anantitumor effect against solid tumors in vitro and in vivo. The aim of the present study was to investigate the effects of hispidulin on the human leukemia cell line in vitro and the underlying mechanisms of its actions on these cells. Our results showed that hispidulin inhibits AML cell proliferation in a dose- and time-dependent manner, and induces cell apoptosis throughan intrinsic mitochondrial pathway. Our results also revealed that hispidulin treatment significantly inhibits extracellular matrix metalloproteinase inducer (EMMPRIN) expression in both tested AML cell lines in a dose-dependent manner, and that the overexpression of EMMPRIN protein markedly attenuates hispidulin-induced cell apoptosis. Furthermore, our results strongly indicated that the modulating effect of hispidulin on EMMPRIN is correlated with its inhibitory effect on both the Akt and STAT3 signaling pathways. 

Retracted: No

PubPeer comments:
 Fig 3C,  Mitochondrial membrane potential as determined by flow cytometry analysis . Despite the different percentages, the 0-Hispidulin results for two cell lines appear to be identical.  , 
 There is uncertainty whether the corresponding email address belongs to the last author of the present paper, or to Yantao Han as in [other papers] .  Could either author clarify? , 
 False alarm - wrong thread. ,
Tumstatin, an endothelial cell-specific inhibitor of protein synthesis
Authors: Nahum Sonenberg
C Ronald Kahn
Yohei Maeshima
Akulapalli Sudhakar
Julie C Lively
Raghu Kalluri
Richard O Hynes
Kohjiro Ueki
Surender Kharbanda
Journal: Science (2002)
Discipline: Multidisciplinary
Keywords: Tumstatin; anti-angiogenic; proapoptotic; endothelial cell-specific inhibitor; protein synthesis
Affiliations: Program in Matrix Biology, Department of Medicine and the Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.

Abstract:  Tumstatin is a 28-kilodalton fragment of type IV collagen that displays both anti-angiogenic and proapoptotic activity. Here we show that tumstatin functions as an endothelial cell-specific inhibitor of protein synthesis. Through a requisite interaction with alphaVbeta3 integrin, tumstatin inhibits activation of focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3-kinase), protein kinase B (PKB/Akt), and mammalian target of rapamycin (mTOR), and it prevents the dissociation of eukaryotic initiation factor 4E protein (eIF4E) from 4E-binding protein 1. These results establish a role for integrins in mediating cell-specific inhibition of cap-dependent protein synthesis and suggest a potential mechanism for tumstatin's selective effects on endothelial cells. 

Retracted: No

PubPeer comments:
 Figure 3C shows a splice in the blot image for phospho Akt that is not evident in the total Akt probing. Can the authors explain?  , 
 Somehow this irregularity was missed by NIH investigators: https: grants.nih.gov grants guide notice-files NOT-OD-20-028.html ,
LINC01638 silencing inhibits cancer cell proliferation in colorectal adenocarcinoma through interaction with RUNX2
Authors: Tian Zhang
Xihua Chen
Dengdi Hu
Wenying Zhuo
Journal: Molecular Medicine Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: lncRNA; LINC01638; colorectal adenocarcinoma; plasma levels; RUNX2
Affiliations: Department of General Surgery, Cixi People's Hospital, Cixi, Zhejiang 315300, P.R. China.

Abstract:  lncRNA LINC01638 has been revealed to play an oncogenic role in triple negative breast cancer. The present study was carried out to investigate the involvement of LINC01638 in colorectal adenocarcinoma. In the present study it was observed that LINC01638 in plasma was upregulated in colorectal adenocarcinoma patients compared to healthy controls. Plasma levels of LINC01638 were affected by tumor size but not by distant metastasis. Plasma levels of Runt‚Äërelated transcription factor 2 (RUNX2) were also higher in colorectal adenocarcinoma patients than in healthy controls, and were positively correlated with plasma levels of LINC01638 in colorectal adenocarcinoma patients but not in healthy controls. ROC curve analysis revealed that upregulation of LINC01638 distinguished colorectal adenocarcinoma at stage I and II from healthy controls. LINC01638 shRNA knockdown led to RUNX2 downregulation, while RUNX2 overexpression exhibited no significant effects on LINC01638. LINC01638 shRNA knockdown inhibited and RUNX2 overexpression promoted the proliferation of colorectal adenocarcinoma cells. RUNX2 overexpression attenuated the effects of LINC01638 shRNA knockdown on cancer cell proliferation. Therefore, lncRNA LINC01638 silencing may inhibit cancer cell proliferation in colorectal adenocarcinoma through its interaction with RUNX2. 

Retracted: Yes

PubPeer comments:
 2021 retraction 10.3892 mmr.2019.10191 Following the publication of the above paper, the authors drew to the Editor s attention that they had identified some errors in Fig. 5A. First, the authors were unable to locate the original images for Fig. 5A; furthermore, repetitions of the same experiments yielded results that were opposite to those that the authors had originally reported. These results were integral to the study, and affected the reported conclusions in the article. Therefore, the authors requested that the paper be withdrawn from the publication. The Editor of Molecular Medicine Reports has considered the authors request, and agrees that the article should be retracted from the Journal. Note that all that authors agree with the retraction of this paper, and the Editor and the authors apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Molecular Medicine Reports 19: 5275-5280, 2019; DOI: 10.3892 mmr.2019.10191] ,
The HPA/SDC1 axis promotes invasion and metastasis of pancreatic cancer cells by activating EMT via FGF2 upregulation
Authors: Haichao Zhao
Haoliang Zhao
Xifeng Fu
Changzhou Chen
Xidong Chen
Jian Li
Jiefeng He
Journal: Oncology Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: epithelial-mesenchymal transition; fibroblast growth factor 2; heparanase; pancreatic cancer; syndecan-1.
Affiliations: Graduate School, Shanxi Medical University, Taiyuan, Shanxi 030000, P.R. China, Department of General Surgery, Shanxi Dayi Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi 030032, P.R. China

Abstract:  Pancreatic cancer is characterized by the absence of early specific clinical symptoms, accompanied with rapid metastasis and invasion. It is one of the most prevalent types of cancer and more importantly, one of the most common types of malignant cancer with the highest mortality rate of all cancer types. The heparanase (HPA)/syndecan-1 (SDC1) axis has been reported to promote tumor growth, invasion, metastasis and angiogenesis in a variety of cancer types; however, studies into the role and mechanism of the HPA/SDC1 axis in pancreatic cancer are limited. The present study aimed to investigate the biological function and clinical significance of the HPA/SDC1 axis in pancreatic cancer. The results demonstrated that HPA is elevated in pancreatic cancer tissues and cell lines, and that its high expression was associated with poor prognosis. HPA was revealed to mediate an increase in fibroblast growth factor 2 (FGF2) expression by upregulating the expression of SDC1. Conversely, silencing HPA mediated the suppression of FGF2 expression. Furthermore, upregulated FGF2 was observed to increase the expression of downstream Palladin proteins by activating the PI3K/Akt signaling pathway and also lead to the activation of epithelial-mesenchymal transition (EMT). Subsequently, EMT was found to promote the migration and invasion of pancreatic cancer cells. In summary, the HPA/SDC1 axis was revealed to serve an important role in the regulation of FGF2, and was found to promote the invasion and metastasis of pancreatic cancer cells. These findings indicated that the HPA/SDC1 axis may be used as an effective therapeutic target for pancreatic cancer. 

Retracted: No

PubPeer comments:
 According to the press, this research was  financed by the Alzheimer s Association and The Jeffrey Epstein VI Foundation amongst others . https: www.prnewswire.com news-releases a-vascular-cause-for-alzheimers-is-revealed-with-the-backing-of-science-investor-jeffrey-epstein-159412485.html This conflicts with the financial statement provided in the article. Could authors please explain this apparent discrepancy?  ,
Signal transduction involved in lipoxin A4‚Äëinduced protection of tubular epithelial cells against hypoxia/reoxygenation injury
Authors: Ming-Jie Wang
Xiao-Qing Chen
Sheng-Hua Wu
Jing L√º
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Lipoxin A4; Renoprotection; Ischemia/reperfusion injury; Renal tubular cells; Hypoxia/reoxygenation injury
Affiliations: Department of Pediatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.

Abstract:  Previous studies have reported that lipoxin A4 (LXA4) may exert a renoprotective effect on ischemia/reperfusion injury in various animal models. The underlying mechanism of LXA4‚Äëinduced renoprotection during ischemia/reperfusion injury remains to be elucidated. The present study investigated LXA4‚Äëinduced protection on renal tubular cells subjected to hypoxia/reoxygenation (H/R) injury, and determined the effects of peroxisome proliferator‚Äëactivated receptor‚ÄëŒ?(PPARŒ≥) and heme oxygenase‚Ä? (HO‚Ä?) on LXA4 treatment. HK‚Ä? human tubular epithelial cells exposed to H/R injury were pretreated with LXA4, signal molecule inhibitors or the HO‚Ä? inhibitor zinc protoporphyrin‚ÄëIX, or were transfected with PPARŒ≥ small interfering RNA (siRNA) or nuclear factor E2‚Äërelated factor 2 (Nrf2) siRNA. The protein and mRNA expression levels of PPARŒ≥ and HO‚Ä? were analyzed using western blotting and reverse transcription‚Äëquantitative polymerase chain reaction. Binding activity of Nrf2 to the HO‚Ä? E1 enhancer was determined using chromatin immunoprecipitation. Nrf2 binding to the HO‚Ä? antioxidant responsive element (ARE) was assessed using electrophoretic mobility shift assay. Preincubation of cells with LXA4 exposed to H/R injury led to a decreased production of inducible nitrogen oxide synthase, malondialdehyde, Œ≥‚Äëglutamyl transpeptidase, leucine aminopeptidase and N‚Äëacetyl‚ÄëŒ≤‚Äëglucosaminidase. In addition, LXA4 pretreatment increased cell viability, protein and mRNA expression levels of PPARŒ≥ and HO‚Ä? and PPARŒ≥ and HO‚Ä? promoter activity. SB20358 is a p38 mitogen‚Äëactivated protein kinase (p38 MAPK) pathway inhibitor, which reduced LXA4‚Äëinduced PPARŒ≥ expression levels. LXA4 treatment upregulated p38 MAPK activation, Nrf2 nuclear translocation and increased binding activity of Nrf2 to HO‚Ä? ARE and E1 enhancer in cells exposed to H/R injury. Transfection of the cells with PPARŒ≥ siRNA reduced the LXA4‚Äëinduced Nrf2 translocation. Transfection of the cells with PPARŒ≥ siRNA or Nrf2 siRNA also reduced the LXA4‚Äëinduced increase in HO‚Ä? expression. In conclusion, LXA4‚Äëinduced protection of renal tubular cells against H/R injury was associated with the induction of PPARŒ≥ and HO‚Ä?, via activation of the p38 MAPK pathway, as well as Nrf2 nuclear translocation and binding to HO‚Ä? ARE and E1 enhancer. Therefore, LXA4‚Äëinduced renoprotection is associated with activation of the p38 MAPK/PPARŒ≥/Nrf2‚ÄëARE/HO‚Ä? pathway. 

Retracted: No

PubPeer comments:
 Unexpected similarities between the EMSA figure in this article and a figure of a previously published article from the same group. ,
Oleate promotes differentiation of chicken primary preadipocytes in¬†vitro
Authors: Hui Li
Zhouchun Shang
Hui Shi
Lin Guo
Ning Wang
Yuxiang Wang
Journal: Bioscience Reports (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: adipogenesis; chicken; differentiation; fatty acid; inducer
Affiliations: Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture, Harbin 150030, People's Republic of China., Key Laboratory of Animal Genetics, Breeding and Reproduction, Education Department of Heilongjiang Province, Harbin 150030, People's Republic of China., College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, People's Republic of China., Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture, Harbin 150030, People's Republic of China    .

Abstract:  In addition to providing energy and constituting cell membrane, fatty acids also play an important role in adipocyte differentiation and lipid metabolism. As an important member of monounsaturated fatty acids, oleate, together with other components, is widely used to induce chicken preadipocyte differentiation. However, it is not clear whether oleate alone can induce chicken preadipocyte differentiation. In the present study, four different treatments were designed to test this question: basal medium, IDX [insulin, dexamethasone and IBMX (isobutylmethylxanthine)], oleate and IDX plus oleate. Cytoplasmic lipid droplet accumulation and mRNA expression for adipogenesis-related genes were monitored. After treatment of oleate on chicken preadipocytes, apparent lipid droplet formation and lipid accumulation were observed, accompanied by increasing expression of PPARŒ≥ (peroxisome proliferator-activated receptor-Œ≥) and AFABP (adipocyte fatty acid-binding protein), but decreasing level of GATA2 (GATA-binding protein 2). In contrast, for cells cultured in the basal medium with or without IDX supplementation, lipid droplet barely occurred. These results suggest that exogenous oleate alone can act as an inducer of preadipocyte differentiation into adipocytes. 

Retracted: No

PubPeer comments:
 Figure 2 appears to have an image overlap. ***  , 
 April 9, 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1
Authors: Yingbiao Wu
Ming Fang
Yanfei Li
Xuejun Wang
Xinming Li
Zhongping Ning
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: atherosclerosis; miR-185; stromal interaction molecule 1.
Affiliations: Department of Cardiology, Hainan General Hospital, Haikou, China, Department of Cardiology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Abstract:  Background: Atherosclerosis (AS) is a major risk factor for cardiovascular disease. microRNAs play a key role in gene regulation in the formation and development of atherosclerotic plaques. Herein, the role and target gene of miR-185 in AS were explored. Materials and methods: Cell viability, migration and invasion were examined by cell counting kit-8 (CCK-8) and transwell assay. The relative luciferase activity was measured by luciferase reporter assay. The levels of miR-185, STIM1, vascular endothelial growth factor (VEGF) and matrix metalloprotein-9 (MMP-9) were evaluated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot. Results: The results revealed that ox-LDL decreased miR-185 expression, and enhanced STIM1 expression in MOVAS cells, as well promoted cell viability, migration and invasion. 3'-UTR of STIM1 contained miR-185 binding site according to the Targetscan. miR-185 silencing or STIM1 overexpression promoted the viability, migration and invasion of ox-LDL-induced MOVAS cells. miR-185 overexpression or STIM1 silencing had the opposite effect. Besides, miR-185 silencing up-regulated the levels of VEGF and MMP-9 in vitro, and increased the lesions of arterial wall tissues and STIM1 positive rate in vivo. However, STIM1 silencing reversed these effects. Conclusions: Sum up, STIM1 was a potential target gene of miR-185 in AS. Knockdown of miR-185 facilitated the progression of AS through enhancing cell proliferation, migration and invasion via targeting STIM1. The research provides a novel view of miR-185/STIM1 axis function in AS development, and this targeting method may prevent and treat AS. 

Retracted: No

PubPeer comments:
 Fig 7b.  STIM1 positive rate was measured by IHC assay .  A minor error, but authors may wish to check. ,