bluuebunny/crossref_metadata_2025_split huggingface dataset:
TMT-based Quantitative Proteomic Analysis Reveals Defense Mechanism of Wheat Against the Crown Rot Pathogen Fusarium Pseudograminearum
Authors: Qiao Fangfang , Yang Xiwen , Xu Fengdan , Huang Yuan , Zhang Jiemei , Song Miao , Zhou Sumei , He Dexian , Zhang Meng 
Published: November 2020

Abstract
Background: Fusarium crown rot a major disease in wheat. However, wheat defense mechanisms remain poorly understood.Results: In this study, we employed tandem mass tag (TMT) quantitative proteomics technology for one disease-susceptible (UC1110 (S1)) and one disease-tolerant wheat cultivar (PI610750 (S2)) inoculated with Fusarium pseudograminearum WZ-8A. Analysis of morphology and physiology showed that average seedling root diameter was significantly decreased 3 days post-inoculation (dpi) in both cultivars. Malondialdehyde content decreased in PI610750 and catalase activity increased in UC1110, indicating that morphology, physiology, and biochemistry differed in both cultivars in response to disease. TMT analysis identified 366 differentially expressed proteins (DEPs) by Gene Ontology enrichment and the Kyoto Encyclopedia of Genes and Genomes in the two comparison groups, S1-3dpi/S1-0dpi (163) and S2-3dpi/S2-0dpi (203). We concluded that phenylpropanoid biosynthesis (8), secondary metabolite biosynthesis (12), linolenic acid metabolites (5), glutathione metabolism (8), plant hormone signal transduction (3), MAPK signaling pathway-plant (4), and photosynthesis (12) contributed to wheat defense mechanisms. Protein-protein interaction network analysis showed that DEPs interacted in sugar metabolism and photosynthesis pathways. We validated 16 genes by real-time quantitative polymerase chain reaction.Conclusion: The results were consistent with proteomics data. Our results provided insight into molecular mechanisms of interaction between wheat and F. pseudograminearum.
Investigating Psychometric Properties of the Arm Activity Measure – Thai Version (ArmA-TH) Sub-scales Using the Rasch Model
Authors: Buntragulpoontawee Montana , Khunachiva Jeeranan , Euawongyarti Patreeya , Wongpakaran Nahathai , Wongpakaran Tinakon , Kaewma Atcharee , Ashford Stephen 
Published: November 2020

Abstract
Background: This study investigated the ArmA-TH measurement properties based on item response theory, using the Rasch model. Methods: Patients with upper limb hemiplegia resulting from cerebrovascular and other brain disorders were asked to completed the ArmA-TH questionnaire. Rasch analysis was performed to test how well the ArmA-TH passive and active function sub-scales fit the Rasch model by investigating unidimensionality, response category functioning, reliability of the person and item, and differential item functioning (DIF) for age, sex and education. Results: Participants had stroke or other acquired brain injury (n=185) and the majority were men 126(68.1%), with a mean age of 55(SD 22). Most patients 91(49.2%) graduated elementary/primary school. For the ArmA-TH passive function scale, all items had acceptable fit statistics. The scale’s unidimensionality, and local independence were supported. The reliability was acceptable. Disordered threshold was found in five items, none was DIF. For the ArmA-TH active function scale, one item was misfitting and three were locally dependent. The reliability was good. DIF was not found. All items had disordered thresholds, and data fitted the Rasch model better after rescoring.Conclusions: Both sub-scales of ArmA-TH fitted the Rasch model, and are valid and reliable. The disordered thresholds should be further investigated.
Immunotherapy Against Acetylated Tau at K280 Ameliorates Behavioral Impairments and Pathologies of Tau Transgenic Mouse
Authors: Kim Na-Young , Song Ha-Lim , Cho Kwangmin , Shim Young-Lim , Lee Kyounghye , Mun Yeon-Seon , Lee Seung-Eun , Kim Min-Seok , Kim Hyun-Ju , Kim Dong-Hou , Yoon Seung-Yong 
Published: November 2020

Abstract
Background : Tau is gaining attention as a target of therapeutic antibodies for Alzheimer's disease (AD) and other tauopathies but it was recently of debate which epitope on tau has therapeutic potency. While the hexapeptide 275VQIINK280 is a critical region for tau aggregation and K280 is acetylated in various tauopathies including AD, there has been no immunotherapy targeting acetylated K280. Methods : Acetylated K280 was first chosen as therapeutic target from small pilot studies comparing in vivo behavioral efficacy of tau transgenic mice by immunizing with several putatively pathogenic epitopes such as acetylated or phosphorylated or cleaved tau. Results : Therapeutic efficacy in tau transgenic mice was further evaluated with behavior, pathology and biochemical experiments after either active immunization with tau peptide acetylated at K280 or passive immunization with anti-tau antibody targeting K280 acetylation. Vaccination with tau peptide acetylated at K280 or antibody (Y01) targeting it ameliorated memory impairments and pathology in tau transgenic mice via intracerebroventricular or intraperitoneal route. Conclusions : This study showed that acetylated K280 tau is a good therapeutic target and Y01 could be a novel therapeutic antibody for AD and other tauopathies.
Could the Perioperative Use of Opioids Influence Cancer Outcomes After Surgery? A Scoping Review Protocol
Authors: Cascella Marco , Cuomo Arturo , Bifulco Francesca , Caprio Barbara Di , Accardo Rosanna , Forte Cira Antonietta , Esposito Gennaro , Fiore Marco 
Published: November 2020

Abstract
BackgroundOpioids are commonly used for the treatment of cancer and non-cancer pain, and during and after general anesthesia. Because preclinical studies underlined a potential opioid-mediated immunosuppression, it was postulated that the perioperative administration of opioids could influence cancer outcomes after surgery. Nevertheless, clinical data have been extrapolated mainly from retrospective analyses. Thus, the precise link between perioperative opioids use and cancer recurrence/metastasis or cancer-related mortality/morbidity remains unresolved.Methods/designThis scoping review is planned following the Joanna Briggs Institute recommendations. The authors will conduct a literature review through the PRISMA statement using PubMed and EMBASE databases; the Grey literature will be explored using Google Scholar, Conference Proceedings Citation Index (via Web of Science) and Open Grey. The search strategy will be limited to articles published in the English language and to human studies. The database searches are planned from the inception to November 2020. Two reviewers will independently screen titles and abstracts, followed by a full-text screening of potentially relevant articles with standardized data extraction. Any disagreement for the inclusion between the two reviewers will be discussed with a third reviewer.DiscussionThe review aim to map the available literature focusing on a possible association between the perioperative opioids use and cancer outcomes in patients undergoing surgery. The proposed approach will allow to identify and analyze the knowledge gap in the field and, serving as a prerequisite for future research including systematic reviews and clinical studies.Scoping review registrationOpen Science Framework https://osf.io/ng57c/ DOI 10.17605/OSF.IO/NG57C
rAAV-Delivered PTEN Therapeutics for Prostate Cancer
Authors: Ai Jianzhong , Li Jia , Su Qin , Ma Hong , He Ran , Wei Qiang , Li Hong , Gao Guangping 
Published: November 2020

Abstract
Background: Prostate cancer (PCa) is the second most popular diagnosed cancer and the fifth leading cause of cancer-related mortality for males globally. At present, effective treatments for PCa need to be further developed. To further understand the molecular mechanism and develop novel therapeutics for PCa, the role of phosphatase and tensin homolog (PTEN) signaling in PCa progression was investigated. Previous studies have reported that PTEN and its downstream target cyclin-dependent kinase inhibitor 1B (CDKN1B) are significantly downregulated in PCa cells compared to normal controls; therefore, modulation of PTEN and CDKN1B expression might be a promising therapeutic approach for PCa treatment. Methods: The expression of PTEN and CDKN1B was first verified in specimens from PCa patients or transgenic adenocarcinoma mouse prostate (TRAMP) mice. The effect of PTEN on PCa cell migration, apoptosis and cell cycle was analyzed by wound healing assay and flow cytometry in vitro. Next, we tested the concept of intraprostatic and intratumoral injection of recombinant adeno-associated virus (rAAV) 9 expressing Pten or Cdkn1b (4x1011 genome copies (GCs)/prostate) into 8-week-old TRAMP mice and a subcutaneous tumor xenograft mouse model (5x1011 GCs/tumor), respectively, to inhibit PCa progression. Results: PTEN and CDKN1B were significantly downregulated in human and mouse PCa samples, and CDKN1B expression was positively correlated with PTEN expression. Further, PTEN overexpression significantly inhibited the cell migration and cell cycle progression and promoted the apoptosis of PCa cells by decreasing Ccnd1 expression and increasing Cdkn1b expression. Importantly, rAAV9.Pten or rAAV9.Cdkn1b treatment significantly extended the lifespan of TRAMP mice and inhibited the growth rate of tumor xenografts by regulating downstream gene expression. Moreover, we confirmed that neoplasia in the treated prostates was significantly diminished compared to that in the control prostates and that apoptosis was markedly observed in xenografts treated with Pten or Cdkn1b, highlighting changes in two crucial factors for PCa progression. Conclusions: Taken together, these data indicate that rAAV-based PTEN/CDKN1B delivery holds promise for the development of novel therapeutics for PCa.
Sulforaphane Activates Brain-Derived Neurotrophic Factor (BDNF) Transcription by NF-E2-Related factor-2 (Nrf2), Showing Prevention Effects on the Microglial of Stressed Mice
Authors: Tang Rui , Cao Qianqian , He Lujuan , Du Pengfei , Chen Gang , Fu Rao , Xiao Fei , Sun Yirong , Zhang Ji-chun 
Published: November 2020

Abstract
Background: Accumulating evidence suggested that sulforaphane (SFN) showed prevention effects in stressed mice by activating the NF-E2-related factor-2 (Nrf2). However, the mechanism remains poorly understood. The present study aimed to investigate whether the prevention effects of SFN in stressed mice by activating brain-derived neurotrophic factor (BDNF) transcription on the microglial and revising abnormal dendritic spine morphology. Methods: In vitro study, we performed the Luciferase assay, Chromatin immunoprecipitation assay, Immunofluorescence, and Western blot to investigate whether SFN could activate Nrf2, resulting in BDNF transcription on the BV2 cell. In vivo study, we employed the Social defeat stress mice model, Behavior test, Western blots, Immunofluorescence, and Enzyme-linked immunosorbent assay to further explore whether the prevention effects of SFN in stressed mice by activating BDNF transcription on the microglial and revising abnormal dendritic spine morphology.Results: First, we found that SFN could activate Nrf2, resulting in Nrf2 binding to the BDNF exon I promoter, leading to BDNF protein expression on the BV2 cell. Second, SFN attenuated the decreased levels of Nrf2, and increased levels of MeCP2 expression, revising abnormal BDNF expression in the stressed mice. Third, we further found that the SFN could attenuate the decreased levels of Nrf2 and increased levels of MeCP2 expression on the microglial and revising microglial dysfunction in the stressed mice. Fourth, SFN could attenuate the increased levels of pro-inflammatory cytokine and the decreased levels of anti-inflammatory cytokine release in the stressed mice. Finally, SFN showed prevention effects and revised abnormal dendritic spine morphology in the stressed mice. Conclusions: Therefore, the prophylactic effects of SFN in the stressed mice by activating BDNF transcription on the microglial and revising abnormal dendritic spine morphology.
Betulinic Acid Inhibits ROS-Mediated Pyroptosis in Spinal Cord Injury by Augmenting Autophagy via the AMPK-mTOR-TFEB Signaling Pathway
Authors: Wu Chenyu , Chen Huanwen , Zhuang Rong , Wang Yongli , Hu Xinli , Zhang Haojie , Xu Yu , Li Jiafeng , Li Yao , Xu Huazi , Xu Hui , Ni Wenfei , zhou kailiang 
Published: November 2020

Abstract
Background：Spinal cord injury (SCI) results in a wide range of disabilities. Its complex pathophysiological process limits the effectiveness of many clinical treatments. Betulinic acid (BA) has been shown to be an effective treatment for some neurological diseases, but it has not been studied in SCI. In this study, we assessed the role of BA in SCI and investigated its underlying mechanism. Methods：Using a mouse model of SCI, survival and functional outcomes following injury were assessed. Western blotting, ELISA, and immunofluorescence techniques were employed to analyze levels of autophagy, mitophagy, and pyroptosis; ROS- and AMPK-related signaling pathways were also examined. Results：Our results showed that BA significantly improves functional recovery following SCI. Furthermore, autophagy, mitophagy, ROS-activity and pyroptosis were implicated in the mechanism of BA in the treatment of SCI. Specifically, our results suggest that BA restored autophagy flux following injury, which induces mitophagy to eliminate the accumulation of ROS and subsequently inhibits pyroptosis. Further mechanistic studies revealed that BA likely regulates autophagy and mitophagy via the AMPK-mTOR-TFEB signaling pathway. Conclusion: BA can significantly promote the recovery following SCI and that it may be a promising therapy for SCI.
Cytochrome P450-Epoxygenated Fatty Acids Inhibit Müller Glial Inflammation
Authors: Ontko Cayla D. , Capozzi Megan E. , Kim Minjae J. , McCollum Gary W. , Penn John S. 
Published: November 2020

Abstract
BackgroundMüller cell (MC) inflammation is an early pathogenic step in the vision-threatening disease diabetic retinopathy (DR). Recent evidence indicates that diabetes-induced free fatty acid (FFA) dysregulation can elicit the release of inflammatory cytokines from MC, promoting DR progression. Palmitic acid (PA) is elevated in the sera of diabetics and stimulates the production of the DR-relevant cytokines by MC, including interleukin-1β (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNFα). IL-1β is elevated in DR and is purported to be a “master regulator” of cytokine-induced inflammation. IL-1β activates MC to produce itself (IL-1β auto-amplification) and other inflammatory cytokines in the retina. Consequently, a modality that blocks both FFA- and IL-1β-induced MC inflammation has therapeutic potential in DR. The CYP-derived epoxygenated fatty acids, epoxyeicosatrienoic acid (EET) and epoxydocosapentaenoic acid (EDP), offer one such therapeutic strategy. In this study we propose that experimental elevation of EET and EDP will reduce PA- and IL-1β-induced MC inflammation.MethodsHuman MC (hMC) were treated with vehicle, broad-spectrum CYP inhibitor SFK-525a, or PA or IL-1β in the presence or absence of 11,12-EET, 19,20-EDP or GSK2256294, a soluble epoxide hydrolase (sEH) inhibitor. Relative expression of TNFα, IL-1β, IL-6, and IL-8 was assayed via qRT-PCR and NFκB-dependent transcription was tested using a luciferase assay. Data were analyzed using ANOVA with Tukey’s multiple comparisons post-hoc test. ResultsCYP inhibition by SKF-525a increased hMC expression of inflammatory cytokines. Exogenous 11,12-EET and 19,20-EDP both significantly decreased PA- and IL-1β-induced hMC expression of IL-1β and IL-6. Both epoxygenated fatty acids significantly decreased IL-8 expression in IL-1β-induced hMC and TNFα in PA-induced hMC. Interestingly, 11,12-EET and 19,20-EDP significantly increased TNFα in IL-1β-treated hMC. GSK2256294 significantly reduced PA- and IL-1β-stimulated hMC cytokine expression, demonstrating efficacy over a range of concentrations. 11,12-EET and 19,20-EDP were also found to decrease PA- and IL-1β-induced NFκB-dependent transcriptional activity.ConclusionsIn summary, these data suggest that experimental elevation of 11,12-EET and 19,20-EDP decreases MC inflammation occurring under diabetes-relevant conditions and may represent a viable therapeutic strategy for inhibition of early retinal inflammation in DR. Our data suggest that these epoxygenated fatty acids exert their anti-inflammatory activities, at least in part, by blocking NFκB-dependent transcription.
Upregulation of ICAM-1 and HLA-G Genes Expression in Cumulus Cells of Infertile Women with Poor Response to Ovarian Stimulation with a Healthy Lifestyle
Authors: Aftabsavad Somayeh , Noormohammadi Zahra , Moini Ashraf , Karimipoor Morteza 
Published: November 2020

Abstract
Purpose: Diagnosis of women with poor ovarian response (POR) to exogenous gonadotropin stimulation is a challenge for reproductive specialists. This study aimed to investigate the expression profile for ICAM-1 and HLA-G genes in the cumulus cells of infertile women with POR based on their healthy lifestyle. Methods: Eighty women under the age of 35 were enrolled and divided into two groups: 1- POR without a healthy lifestyle (n=40) and POR with a healthy lifestyle (n=40). The ICAM-1 and HLA-G genes expression was compared by the quantitative PCR between the groups. The ICAM-1 and HLA-G protein levels were analyzed by the western blotting technique, and the methylation pattern was investigated by the methylation-specific PCR.Results: The qRT-PCR assay showed that ICAM-1 and HLA-G genes were differentially expressed between the two groups studied. ICAM-1,HLA-G genes,and proteins expressions in POR with healthy lifestyle were upregulated compared to the second group (P<0.05). ICAM-1 and HLA-G DNA methylation status in the POR with a healthy lifestyle were decreased compared to the other group (P<0.05). The oocyte quality and clinical pregnancy ratio were significantly higher in the POR with a healthy lifestyle women than in the other ones (P<0.05). Conclusion: Theupregulation of ICAM-1 and HLA-G in POR women is probably related to lifestyle. Lifestyle may affect the methylation pattern, protein levels and alteration of gene expression profiles in the cumulus cells of POR women. Additionally, lifestyle may be considered a marker for ovulation, oocyte maturation, preimplantation and clinical pregnancy process.
CircRNA&nbsp;circFADS2&nbsp;is Under-expressed in Sepsis and Protects Lung Cell From LPS-induced Apoptosis by Downregulating miR-133a
Authors: Niu Fang , Liang Xiaofeng , Ni Jindi , Xia Zhuye , Jiang Lijing , Wang Hong , Liu Hongjie , Shen Guofeng , Li Xiang 
Published: November 2020

Abstract
Background: It has been reported that circFADS2 and miR-133a play opposite roles in LPS-induced cell apoptosis, which contributes to the development of sepsis. This study was carried out to explore the interaction between circFADS2 and miR-133a in sepsis. Methods: Expression of circFADS2 and miR-133a in plasma from both sepsis patients (n=62) and healthy controls (n=62) was studied by RT-qPCR. The effects of LPS on the expression of circFADS2 and miR-133a were also analyzed by RT-qPCR. The crosstalk between circFADS2 and miR-133a was analyzed by overexpression, followed by RT-qPCR. The role of circFADS2 and miR-133a in regulating the apoptosis of lung cells induced by LPS was analyzed by cell apoptosis assay.Results: We found that circFADS2 was under-expressed in sepsis and miR-133a was overexpressed in sepsis. An inverse correlation between circFADS2 and miR-133a was observed across sepsis samples. In lung cells, LPS treatment decreased the expression of circFADS2 and increased the expression of miR-133a. In lung cells, circFADS2 overexpression decreased the expression of miR-133a. Moreover, circFADS2 overexpression reduced the enhancing effects of miR-133a overexpression on cell apoptosis induced by LPS. Conclusion: Therefore, circFADS2 is under-expressed in sepsis and may protect lung cell from LPS-induced apoptosis by downregulating miR-133a.
Treatment of Venous Thromboembolism in Cancer Patients: A Systemic Review and Meta-analysis on the Efficacy and Safety of Different DOACs
Authors: Song Xiaojun , Liu Zhili , Zeng Rong , Shao Jiang , Liu Bao , Zheng Yuehong , Liu Changwei , Ye Wei 
Published: November 2020

Abstract
Background: To evaluate the efficacy and safety of different direct oral anticoagulants (DOACs) compared with low molecular weight heparin (LMWHs) in the treatment of venous thromboembolism (VTE) in cancer patients.Methods: Literature was searched in databases including Cochrane Library, EMBASE (Ovid) and MEDLINE (Pubmed). Eligible studies were included and data were collected independently by two reviewers. We conducted a systemic review of the efficacy and safety of DOACs in the treatment of VTE in cancer patients. The odds ratios of different DOACs compared with LMWHs for VTE, DVT, PE recurrences, major bleeding and clinically relevant non-major bleeding (CRNMB) were calculated in meta-analyses and subgroup analyses.Results: A total of 18 articles were eligible for analyses, including 4 randomized controlled trials (RCTs) and 14 retrospective studies. Both RCTs and retrospective studies confirmed that DOACs decreased the risk of VTE recurrence (RCTs: OR, 0.60; 95%CI, 0.45-0.80; retrospective studies: OR, 0.73; 95%CI, 0.59-0.90) and DVT recurrence (RCTs: OR, 0.54; 95%CI, 0.36-0.80; retrospective studies: OR, 0.20; 95%CI, 0.06-0.63), but not PE recurrence or fatal PE in cancer patients. Subgroup analyses revealed an important role of rivaroxaban in decreasing recurrent VTE. Meanwhile, major bleeding events were not increased in the DOAC group, but the risk of CRNMBs were significantly elevated. Subgroup analyses confirmed the role of rivaroxaban in increasing the risk of major bleeding events and CRNMBs. Conclusions: Compared with LMWHs, DOACs, especially rivaroxaban, significantly reduced the risk of VTE and DVT, rather than PE, recurrence in patients with cancer. Although DOACs did not increase the major bleeding events in pooled analysis, rivaroxaban was showed an elevated risk of this adverse effect in subgroup analysis. In addition, the risk of CRNMB events was increased after the application of DOACs including rivaroxaban.
Warfarin Versus Direct Oral Anticoagulants for Treating Left Ventricular Thrombus: A Systematic Review and Meta-Analysis
Authors: Dalia Tarun , Lahan Shubham , Ranka Sagar , Goyal Amandeep , Zoubek Sara , Gupta Kamal , Shah Zubair 
Published: November 2020

Abstract
Background: Left ventricular thrombus (LVT) is not uncommon and pose a risk of systemic embolism, which can be mitigated by adequate anticoagulation. Direct oral anticoagulants (DOACs) are increasingly being used as alternatives to warfarin for anticoagulation, but their efficacy and safety profile has been debated. We aim to compare the therapeutic efficacy and safety of DOACs versus warfarin for the treatment of LVT.Methodology: We systematically searched PubMed/Medline, Google Scholar, Cochrane library, and LILCAS databases from inception to 14th August 2020 to identify relevant studies comparing warfarin and DOACs for LVT treatment and used the pooled data extracted from retrieved studies to perform a meta-analysis.Results: We report pooled data on 1955 patients from 8 studies, with a mean age of 61 years and 59.7 years in warfarin and DOACs group, respectively. The pooled odds ratio for thrombus resolution was 1.11 (95% CI 0.51–2.39) on comparing warfarin to DOAC, but it did not reach a statistical significance (p = 0.76). The pooled risk ratio (RR) of stroke or systemic embolization and bleeding in patients treated with warfarin vs DOACs was 1.04 (95% CI 0.64–1.68; p = 0.85), and 1.15 (95% CI 0.62–2.13; p = 0.57), respectively; with an overall RR of 1.09 (95% CI 0.70–1.70; p =0.48) for mortality.Conclusions: DOACs appears to be non-inferior or at least as effective as warfarin in the treatment of left ventricular thrombus without any statistical difference in stroke or bleeding complications.