bluuebunny/crossref_metadata_2025_split huggingface dataset:
A small‐scale investigation process for the Clostridium acetobutylicum production of butanol using high‐energy carbon heavy ion irradiation
Authors: Jiang Ting‐Ting , Zhou Xiang , Liang Yan 
Published: September 2018

AbstractApplied heavy ion irradiation technology and butanol industrial practices as a whole have been used as a strategy for the development of an attractive alternative to petroleum‐based fuels. Clostridium acetobutylicum (C. acetobutylicum) strains are well documented as fermentation strains for the production of biobutanol. However, it has been reported that solvent production inhibits the growth of these strains, and the accumulation of acetate also inhibits biomass synthesis, rendering the production of butanol from acetone‐butanol‐ethanol (ABE) fermentation processes economically challenging. In this manuscript, we propose the use of high‐energy carbon heavy ion irradiation from the Heavy Ion Research Facility in Lanzhou (HIRFL) to obtain a culture with an increased butanol yield. Our findings suggest that the use of a high‐energy 12C6+ heavy ion irradiation dose of 45 Gy with an energy of 135 AMeV and ion pulses/levels of 106–108 favours ABE solvent production in an irradiated strain compared with the non‐irradiated strain. The strategy reported in this manuscript may contribute to the development of a cost‐effective butanol fermentation process that is competitive with similar fermentation processes.
The Evaluation Landscape: U.S. Foundation Spending on Evaluation
Authors: Kinarsky Alana R. 
Published: September 2018

AbstractFoundations annually distribute over $60 billion to nonprofit organizations. In exchange for funding, nonprofits are often required to evaluate their work by collecting and sharing data that demonstrates their progress and impact. Accordingly, foundations and nonprofits represent a meaningful influence on the evaluation market. The present chapter first describes the historical development of foundations, their important role in society, and their use of evaluation. Informed by this historical account; the chapter then provides an overview of foundation spending on evaluation, detailing the number of evaluation‐related grants and funds allocated by year and by select foundations. In conclusion, the chapter considers implications for the profession and practice of evaluation and offers suggestions for future areas of research.
The Evaluation Marketplace and Its Industry
Authors: Nielsen Steffen Bohni , Lemire Sebastian , Christie Christina A. 
Published: September 2018

AbstractThe present chapter provides the conceptual foundation on which the remainder of this special issue is grounded. First, the chapter considers the idea of an evaluation marketplace and reflects on the limited attention awarded to the commercial aspects of evaluation. Second, the scarce—yet significant—literature on the evaluation market and industry is considered, identifying three distinct strands of contributions: the evaluation market composition, market dynamics, and strategies for navigating these. In the third section, the chapter offers working definitions of the evaluation market and evaluation services as well as presents the evaluation market framework, an emerging framework for better understanding the central components of the evaluation marketplace, including its context, composition, and dynamics. A brief set of concluding notes brings the chapter to a close.
Inside Front Cover: Selective and sensitive Escherichia coli detection based on a T4 bacteriophage‐immobilized multimode microfiber (J. Biophotonics 9/2018)
Authors: Li Yanpeng , Ma Hui , Gan Lin , Gong Andong , Zhang Haibin , Liu Deming , Sun Qizhen 
Published: September 2018

Sensitive Escherichia coli detection based on a T4 bacteriophageimmobilized multimode microfiber is proposed and demonstrated in this article. Different modes are excited and guided in the microfiber as evanescent field that can interact with surrounding E. coli directly. The change of E. coli concentration and corresponding binding of E. coli on microfiber surface will lead to the shift of optical spectrum, which can be exploited for the application of biosensing.Further details can be found in the article by Yanpeng Li, Hui Ma, Lin Gan, et al. (e201800012).
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Inside Cover: Fiber‐based fluorescence lifetime imaging of recellularization processes on vascular tissue constructs (J. Biophotonics 9/2018)
Authors: Alfonso‐Garcia Alba , Shklover Jeny , Sherlock Benjamin E. , Panitch Alyssa , Griffiths Leigh G. , Marcu Laura 
Published: September 2018

Tissue autofluorescence provides fluorescence lifetime contrast between acellular tissue and that containing newly seeded cells. Fiber‐based fluorescence lifetime imaging (FLIm) can be used for tracking recellularization of engineered vascular grafts and potential matrix remodeling at large scale, without compromising sample integrity. FLIm cellular contrast was verified in a subset of samples seeded with eGFP‐labelled cells. Results suggests fiberbased FLIm is a suitable tool for monitoring recellularization of engineered tissue nondestructively.Further details can be found in the article by Alba Alfonso‐Garcia, Jeny Shklover, Benjamin E. Sherlock, et al. (e201700391).
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Association of serum neuron‐specific enolase and bilirubin levels with cerebral dysfunction and prognosis in large‐artery atherosclerotic strokes
Authors: Wang Yan , Xu Shuping , Pan Shengying , Ouyang Hezhong , Zang Zhizhong , Tan Jing 
Published: September 2018

AbstractPurposeTo explore the association of serum neuron‐specific enolase (NSE) and bilirubin levels with cerebral dysfunction in the prognosis of large‐artery atherosclerotic (LAA) stroke cases.MethodsThis study included 73 patients who suffered from LAA stroke and were divided into experimental group (n = 41) that had an increased serum NSE and bilirubin level, and control group (n = 32). At day 1, 7, and 14, the National Institutes of Health Stroke Scale (NIHSS) score, serum NSE, and bilirubin levels were measured. The modified Rankin Scale (mRS) was used to assess neurological functional recovery at 30 days. The good outcome rate was analyzed and tested using the Kaplan‐Meier product‐limit method and the log‐rank test one year afterwards as a follow‐up.ResultsThe NIHSS scores, serum bilirubin, and NSE levels in the experimental group were significantly increased than that of control group at days 1, 7, and 14. There was a remarkable difference in the mRS scores and the good outcome rates between the two groups. Furthermore, the computed tomography detection rate of large‐area cerebral infarctions was higher in the experimental group than that of control group.ConclusionHigh serum NSE levels and hyperbilirubinemia might be biomarkers for a poor prognosis in the early identification of LAA strokes.
Taxifolin prevents postprandial hyperglycemia by regulating the activity of α‐amylase: Evidence from an in vivo and in silico studies
Authors: Rehman Kanwal , Chohan Tahir Ali , Waheed Iqra , Gilani Zeeshan , Akash Muhammad Sajid Hamid 
Published: September 2018

AbstractThere has been a dramatic increase in the prevalence of diabetes mellitus (DM) and its associated complications globally. The postprandial stage of DM involves prompt elevation in the levels of blood glucose and α‐amylase, a carbohydrate‐metabolizing enzyme is mainly involved in the regulation of postprandial hyperglycemia. This study was designed to assess the ability of a well‐known flavonoid, taxifolin (TFN), against postprandial hyperglycemia and its inhibitory effects on α‐amylase activity through the assessment of therapeutic potentials of TFN in an alloxan‐induced diabetic animal model. The binding potential TFN with an α‐amylase receptor was also investigated through molecular dynamics (MD) simulation and docking of to compare the binding affinities and energies of TFN and standard drug acarbose (ACB) with target enzyme. TFN significantly improved the postprandial hyperglycemia, lipid profile, and serum levels of α‐amylase, lipase, and C‐reactive protein in a dose‐dependent manner when compared with that of either DM‐induced and ACB‐treated alloxan‐induced diabetic rats. Moreover, TFN also enhanced the anti‐oxidant status and normal functioning of the liver in alloxan‐induced diabetic rats more efficiently as compared to that of ACB‐treated alloxan‐induced diabetic rats. Therapeutic potentials of TFN were also verified by MD simulation and docking results, which exhibited that the binding energy and affinity of TFN to bind with receptor was significantly higher as compared to that of ACB. Hence, the results of this study signify that TFN might be a potent inhibitor of α‐amylase that has the potential to regulate the postprandial hyperglycemia along with its anti‐inflammatory and anti‐oxidant properties during the treatment of DM.
Lipophilic statins antagonistically alter the major epithelial‐to‐mesenchymal transition signaling pathways in breast cancer stem–like cells via inhibition of the mevalonate pathway
Authors: Koohestanimobarhan Soheila , Salami Siamak , Imeni Vahideh , Mohammadi Zeinab , Bayat Omid 
Published: September 2018

AbstractResistance to therapies, recurrence, and metastasis remain challenging issues for breast cancer patients, particularly for triple‐negative and breast cancer stem cells. The activation of the epithelial‐to‐mesenchymal transition (EMT) plays an indispensable role in the poor prognosis of those types. The accumulating proofs indicated that the mevalonate pathway crucially mediates a poor prognosis. Here, the effects of lipophilic 3‐hydroxy‐3‐methyl‐glutaryl‐coenzyme A inhibitors, atorvastatin, lovastatin, and simvastatin, were investigated on expression and function of a selected profile of EMT‐related genes in breast cancer stem–like cells. A nontoxic dose of statins (5 μM for 4 days) significantly (P < 0.05 and >2‐fold change) altered expression of 50 of 71 studied genes with a shared cluster of 37 genes that are coding chief operator of signaling pathways in Hippo, Notch, Wnt, proliferation, invasion, angiogenesis, and cell death. They also significantly decreased the levels of Yap/Taz proteins and shifted the expression of vimentin/E‐cadherin in favor of induction of differentiation. Statins significantly chemosensitized the treated cells to doxorubicin and also reduced in vitro migration of the cells. Whereas lovastatin and simvastatin significantly decreased the expression of CD44, atorvastatin drastically increased CD24 and caused more wide‐ranging impacts. In summary, the statins hold back the process of EMT by the antagonizing of EMT‐promoting pathways. High degree of overlapping findings is supportive of the central role of the mevalonate pathway in cancer stem–like cells, but further studies are required to find the optimized chemical structure for the maximum abrogation of orchestrated EMT pathways.
Vitamin C counteracts miR‐302/367‐induced reprogramming of human breast cancer cells and restores their invasive and proliferative capacity
Authors: Ramezankhani Bahareh , Taha Masoumeh F. , Javeri Arash 
Published: September 2018

AbstractEpigenetic reprogramming by embryonic stem cell‐specific miR‐302/367 cluster has shown some tumor suppressive effects in cancer cells of different tissues such as skin, colon, and cervix. Vitamin C has been known as a reprogramming enhancer of human and mouse somatic cells. In this study, first we aimed to investigate whether exogenous induction of miR‐302/367 in breast cancer cells shows the same tumor suppressive effects previously observed in other cancer cells lines, and whether vitamin C can enhance reprogramming of breast cancer cells and also improve the tumor suppressive function of miR‐302/367 cluster. Overexpression of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells upregulated expression of miR‐302/367 members and also some core pluripotency factors including
OCT4A,
SOX2 and
NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines. However, treatment of the miR‐302/367 transfected cells with vitamin C suppressed the expression of pluripotency factors and augmented the tumorigenicity of the breast cancer cells by restoring their proliferative and invasive capacity and compromising the apoptotic effect of miR‐302/367. Supplementing the culture medium with vitamin C downregulated expression of
TET1 gene which seems to be the reason behind the negative impact of vitamin C on the reprogramming efficiency of miR‐302/367 cluster and its anti‐tumor effects. Therefore application of vitamin C may not always serve as a reprogramming enhancer depending on its switching function on
TET1. This phenomenon should be carefully considered when considering a reprogramming strategy for tumor suppression.
Endotoxin regulates matrix genes increasing reactive oxygen species generation by intercellular communication between palmitate‐treated hepatocyte and stellate cell
Authors: Dornas Waleska , Glaise Denise , Bodin Aude , Sharanek Ahmad , Burban Audrey , Le Guillou Dounia , Robert Sacha , Dutertre Stephanie , Aninat Caroline , Corlu Anne , Lagente Vincent 
Published: September 2018

AbstractPrevious studies have shown that gut‐derived bacterial endotoxins contribute in the progression of simple steatosis to steatohepatitis, although the mechanism(s) remains inaccurate to date. As hepatic stellate cells (HSC) play a pivotal role in the accumulation of excessive extracellular matrix (ECM), leading to collagen deposition, fibrosis, and perpetuation of inflammatory response, an in vitro model was developed to investigate the crosstalk between HSC and hepatocytes (human hepatoma cell) pretreated with palmitate. Bacterial lipopolysaccharide (LPS) stimulated HSC with phosphorylation of the p38 mitogen‐activated protein kinase/NF‐κB pathway, while several important pro‐inflammatory cytokines were upregulated in the presence of hepatocyte–HSC. Concurrently, fibrosis‐related genes were regulated by palmitate and the inflammatory effect of endotoxin where cells were more exposed or sensitive to reactive oxygen species (ROS). This interaction was accompanied by increased expression of the mitochondrial master regulator, proliferator‐activated receptor gamma coactivator alpha, and a cytoprotective effect of the agent N‐acetylcysteine suppressing ROS production, transforming growth factor‐β1, and tissue inhibitor of metalloproteinase‐1. In summary, our results demonstrate that pro‐inflammatory mediators LPS‐induced promote ECM rearrangement in hepatic cells transcriptionally committed to the regulation of genes encoding enzymes for fatty acid metabolism in light of differences that might require an alternative therapeutic approach targeting ROS regulation.
SIRT6 overexpression inhibits cementogenesis by suppressing glucose transporter 1
Authors: Huang Liyuan , Sun Hualing , Song Fangfang , Cao Zhengguo , Jiang Xinquan , Zhang Lu , Li Zhelun , Huang Cui 
Published: September 2018

AbstractCementum, which shares common features with bone in terms of biochemical composition, is important for the homeostasis of periodontium during periodontitis and orthodontic treatment. Sirtuin 6 (SIRT6), as a member of the sirtuin family, plays key roles in the osteogenic differentiation of bone marrow mesenchymal stem cells. However, the involvement of SIRT6 in cementoblast differentiation and mineralization and the underlying mechanisms remain unknown. In this study, we observed that the expression of SIRT6 increased during cementoblast differentiation initially. Analysis of the gain‐ and loss‐of‐function indicated that overexpressing SIRT6 in OCCM‐30 cells suppresses cementoblast differentiation and mineralization and downregulating SIRT6 promotes cementogenesis. GLUT1, a glucose transporter necessary in cementogenesis, was inhibited by SIRT6. Overexpressing GLUT1 in SIRT6‐overexpressed OCCM‐30 cells rescued the inhibitory effect of SIRT6 on cementoblast differentiation and mineralization. Moreover, AMPK was activated after overexpressing SIRT6 and inhibited cementoblast differentiation and mineralization. Downregulating the expression of SIRT6 inhibited AMPK activity. Meanwhile, GLUT1 overexpression significantly decreased AMPK activity. Overall, on one hand, SIRT6 inhibited cementoblast differentiation and mineralization by suppressing GLUT1. On the other hand, SIRT6 inhibited cementoblast differentiation and mineralization by activating the AMPK pathway. GLUT1 overexpression also rescued the increased AMPK pathway activated by SIRT6.
Mitochondrial dysfunction in human immunodeficiency virus‐1 transgenic mouse cardiac myocytes
Authors: Cheung Joseph Y. , Gordon Jennifer , Wang JuFang , Song Jianliang , Zhang Xue‐Qian , Prado Fabian Jana , Shanmughapriya Santhanam , Rajan Sudarsan , Tomar Dhanendra , Tahrir Farzaneh G. , Gupta Manish K. , Knezevic Tijana , Merabova Nana , Kontos Christopher D. , McClung Joseph M. , Klotman Paul E. , Madesh Muniswamy , Khalili Kamel , Feldman Arthur M. 
Published: September 2018

AbstractThe pathophysiology of human immunodeficiency virus (HIV)‐associated cardiomyopathy remains uncertain. We used HIV‐1 transgenic (Tg26) mice to explore mechanisms by which HIV‐related proteins impacted on myocyte function. Compared to adult ventricular myocytes isolated from nontransgenic (wild type [WT]) littermates, Tg26 myocytes had similar mitochondrial membrane potential (ΔΨ
m) under normoxic conditions but lower Δ
Ψ
m after hypoxia/reoxygenation (H/R). In addition, Δ
Ψ
m in Tg26 myocytes failed to recover after Ca
2+ challenge. Functionally, mitochondrial Ca
2+ uptake was severely impaired in Tg26 myocytes. Basal and maximal oxygen consumption rates (OCR) were lower in normoxic Tg26 myocytes, and further reduced after H/R. Complex I subunit and ATP levels were lower in Tg26 hearts. Post‐H/R, mitochondrial superoxide (O
2
•–) levels were higher in Tg26 compared to WT myocytes. Overexpression of B‐cell lymphoma 2‐associated athanogene 3 (BAG3) reduced O
2
•– levels in hypoxic WT and Tg26 myocytes back to normal. Under normoxic conditions, single myocyte contraction dynamics were similar between WT and Tg26 myocytes. Post‐H/R and in the presence of isoproterenol, myocyte contraction amplitudes were lower in Tg26 myocytes. BAG3 overexpression restored Tg26 myocyte contraction amplitudes to those measured in WT myocytes post‐H/R. Coimmunoprecipitation experiments demonstrated physical association of BAG3 and the HIV protein
Tat. We conclude: (a) Under basal conditions, mitochondrial Ca
2+ uptake, OCR, and ATP levels were lower in Tg26 myocytes; (b) post‐H/R, Δ
Ψ
m was lower, mitochondrial O
2
•– levels were higher, and contraction amplitudes were reduced in Tg26 myocytes; and (c) BAG3 overexpression decreased O
2
•– levels and restored contraction amplitudes to normal in Tg26 myocytes post‐H/R in the presence of isoproterenol.
8‐Br‐cADPR, a TRPM2 ion channel antagonist, inhibits renal ischemia–reperfusion injury
Authors: Eraslan Ersen , Tanyeli Ayhan , Polat Elif , Polat Elif 
Published: September 2018

AbstractThe transient receptor potential melastatin‐2 (TRPM2) channel belongs to the transient receptor potential channel superfamily and is a cation channel permeable to Na+ and Ca
2+. The TRPM2 ion channel is expressed in the kidney and can be activated by various molecules such as hydrogen peroxide, calcium, and cyclic adenosine diphosphate (ADP)‐ribose (cADPR) that are produced during acute kidney injury. In this study, we investigated the role of 8‐bromo‐cyclic ADP‐ribose (8‐Br‐cADPR; a cADPR antagonist) in renal ischemia–reperfusion injury using biochemical and histopathological parameters. CD38, cADPR, tumor necrosis factor‐α, interleukin‐1β, and myeloperoxidase (inflammatory markers), urea and creatinine, hydrogen peroxide (oxidant), and catalase (antioxidant enzyme) levels that increase with ischemia–reperfusion injury decreased in the groups treated with 8‐Br‐cADPR. In addition, renin levels were elevated in the groups treated with 8‐Br‐cADPR. Histopathological examination revealed that 8‐Br‐cADPR reduced renal damage and the expression of caspase‐3 and TRPM2. Our results suggest that the inhibition of TRPM2 ion channel may be a new treatment modality for ischemic acute kidney injury.
The efficacy of metformin compared with insulin in regulating blood glucose levels during gestational diabetes mellitus: A randomized clinical trial
Authors: Ghomian Nayereh , Vahed Seyede Houra Mousavi , Firouz Samaneh , Yaghoubi Mohammad Ali , Mohebbi Masoud , Sahebkar Amirhossein 
Published: September 2018

AbstractBackgroundInsulin has been a conventional medication in the treatment of female patients suffering from gestational diabetes mellitus (GDM). However, the need for a large number of insulin injections in these patients causes them a lot of discomforts. Recently, an alternative medication, metformin, has received considerable attention in the treatment of GDM. The aim of this study was to compare the efficacy of metformin and insulin in regulating blood glucose levels and fetal outcomes in GDM.MethodsThis randomized clinical trial included 286 pregnant women diagnosed with positive GDM at 24–28 weeks of pregnancy. The subjects were randomly divided into two groups of 143 patients, with one group receiving insulin and the other undergoing a treatment plan using metformin. Fasting plasma glucose (FPG), 2‐hr plasma glucose (PG) and glycated hemoglobin (HbA1c) were recorded twice a month until delivery. Other variables, including birth delivery method, cause of cesarean section, gestational age at the delivery time, birth trauma, Apgar score, birth weight, admission at neonatal intensive care unit (NICU), and neonatal hypoglycemia were also registered.ResultsAge of mother, body mass index, history of diabetes in the family, previous history of GDM, parity, FPG, 1‐ and 2‐hr PG after meals, and 75‐g glucose tolerance test before treatment were not statistically different between the two groups. FPG, PG, and HbA1c did not show significant differences between the two groups after completing the course of treatment. There was also no significant difference between two groups regarding the birth delivery method, the cause of cesarean section, birth trauma, Apgar score, birth weight, admission at NICU, and neonatal hypoglycemia.ConclusionAs mean FPG and 2‐hr PG were not significantly different between the two groups, it seems that metformin can be recommended as an effective substitute for insulin in the treatment of GDM. However, there are still some undesirable risk factors with both treatments that may threaten the mother and the newborn.