bluuebunny/crossref_metadata_2025_split huggingface dataset:
Foreign direct investment with tax holidays and policy uncertainty
Authors: Azevedo Alcino , Pereira Paulo J. , Rodrigues Artur 
Published: October 2018

AbstractWe study foreign direct investment agreements that entitle firms to a lower tax rate during a tax holiday period. Our model considers both finite and uncertain tax holiday period settings. We show that the tax holiday duration may have, for small tax rate reductions, a nonmonotonic effect on the investment timing. For sufficiently high tax reductions, a longer tax holiday speeds up investment. A higher tax reduction during the tax holiday and a lower uncertainty are shown to have a monotonic effect on the threshold, hastening investment. However, in case of a finite tax holiday, for exceptional high salvage values, a higher uncertainty can speed up investment. We show the usefulness of our model to design an optimal incentives package that prompts investment.
Enzalutamide‐induced severe thrombocytopenia complicated by a seizure in a 76‐year‐old man with castration‐resistant prostate cancer
Authors: Murata Masaki , Takizawa Itsuhiro , Maruyama Ryo , Kasahara Takashi , Hara Noboru , Tomita Yoshihiko 
Published: October 2018

IntroductionAdverse events with enzalutamide widely used for men with castration‐resistant prostate cancer are of interest.Case presentationA 76‐year‐old man developed castration‐resistant prostate cancer. He received 160 mg of enzalutamide daily. On the 13th day after treatment, severe thrombocytopenia was observed (platelet count: 1.9 × 104/μL). Normal coagulation and fibrinolytic systems suggested thrombocytopenia induced by enzalutamide. Enzalutamide was withdrawn immediately, and platelet count uneventfully recovered to 7.0 × 104/μL and 28.8 × 104/μL 9 and 30 days after discontinuation, respectively. He restarted enzalutamide therapy without thrombocytopenia recurrence. However, 81 days after restarting enzalutamide, he experienced a seizure. There were no significant findings from brain computed tomography, which suggested that the seizure was also an enzalutamide‐associated adverse event.ConclusionThrombocytopenia may occur early following enzalutamide therapy, and blood analysis within 2 weeks after treatment may facilitate its management. Enzalutamide‐induced thrombocytopenia, complicated by seizure, has not been reported.
Positive deviance, big data, and development: A systematic literature review
Authors: Albanna Basma , Heeks Richard 
Published: October 2018

AbstractPositive deviance is a growing approach in international development that identifies those within a population who are outperforming their peers in some way, eg, children in low‐income families who are well nourished when those around them are not. Analysing and then disseminating the behaviours and other factors underpinning positive deviance are demonstrably effective in delivering development results. However, positive deviance faces a number of challenges that are restricting its diffusion. In this paper, using a systematic literature review, we analyse the current state of positive deviance and the potential for big data to address the challenges facing positive deviance. From this, we evaluate the promise of “big data‐based positive deviance”: This would analyse typical sources of big data in developing countries—mobile phone records, social media, remote sensing data, etc—to identify both positive deviants and the factors underpinning their superior performance. While big data cannot solve all the challenges facing positive deviance as a development tool, they could reduce time, cost, and effort; identify positive deviants in new or better ways; and enable positive deviance to break out of its current preoccupation with public health into domains such as agriculture, education, and urban planning. In turn, positive deviance could provide a new and systematic basis for extracting real‐world development impacts from big data.
Critical success factors for m‐Government adoption in Tanzania: A conceptual framework
Authors: Ishengoma Fredrick , Mselle Leonard , Mongi Hector 
Published: October 2018

AbstractThe advancement of wireless and mobile technologies has given rise to the mobile government (m‐Government). A new channel of public service delivery using a mobile phone. In Tanzania, several m‐Government initiatives have been undertaken. Among these, some can be said to have succeeded while others are still struggling. The reasons for these variations are not known. This study aimed to capture the critical success factors (CSFs) for the adoption of m‐Government and propose a framework under the Tanzanian context. The study builds upon an extensive literature review methodology based on six electronic databases from 2003 to 2017. The results show that security, usability, access, cost, infrastructure, and personal initiatives and characteristics have the strongest effect on the adoption of m‐Government services. Based on the findings of the critical review, a conceptual framework is proposed by extending the mobile services acceptance model (MSAM). A further finding is that most of the m‐Government adoption research have not considered the environmental setting. Hence, this study calls for more research on m‐Government adoption with consideration to the environmental setting (mandatory or optional environment). The study culminates by providing both practical, theoretical, and policy implications of the findings.
Improved ex vivo expansion of mesenchymal stem cells on solubilized acellular fetal membranes
Authors: Shakouri‐Motlagh Aida , O'Connor Andrea J. , Kalionis Bill , Heath Daniel E. 
Published: October 2018

AbstractCoatings produced from extracellular matrixes (ECMs) have emerged as promising surfaces for the improved ex vivo expansion of mesenchymal stem cells (MSCs). However, identifying a readily available source of ECM to generate these coatings is currently the bottleneck of this technology. In this study, we assessed if ECM coatings derived from decellularized fetal membranes were a suitable substrate for MSC expansion. We separated and decellularized the two main components of the fetal membranes, the amnion and the chorion. Characterization of the decellularized membranes revealed that each membrane component has a distinct composition, implying that coatings produced from these materials would have unique biological properties. The membranes were processed further to produce solubilized forms of the decellularized amniotic membrane (s‐dAM) and decellularized chorionic membrane (s‐dCM). On s‐dAM coatings decidual MSCs (DMSC) were more proliferative than those cultured on tissue culture plastic alone or on Matrigel coatings; were smaller in size (a measure of MSC potency); exhibited greater adipogenic differentiation capacity; and improved osteogenic capacity. Additionally, long term culture studies showed late passage DMSCs (passage 8) cultured on s‐dAM showed a decrease in cell diameter over three passages. These data support the use of s‐dAM as a substrate for improved MSC expansion. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 232–242, 2019.
7,8‐Dihydroxy‐3‐(4‐nitrophenyl)coumarin induces cell death via reactive oxygen species–independent S‐phase cell arrest
Authors: Musa Musiliyu A , Gbadebo Akintunde J , Latinwo Lekan M , Badisa Veera LD 
Published: October 2018

AbstractWe herein report the synthesis and in vitro cytotoxicity of 3‐arylcoumarin derivatives (6a‐f and 7a‐f) in human liver (HepG2), prostate (LNCap), and pancreatic (BxPC3) cancer cell lines. Among the tested compounds, 7,8‐dihydroxy‐3‐(4‐nitrophenyl) coumarin (7b) showed the highest cytotoxicity in the HepG2 cell line. The mechanism of cytotoxic action indicated that compound (7b) arrested HepG2 cells at the S phase of the cell cycle progression, induced loss of mitochondrial membrane potential, and caused reactive oxygen species (ROS)‐independent cell death. The cell viability result of pretreated HepG2 cells with antioxidant N‐acetylcysteine followed by compound (7b) treatment and the free radical scavenging activities of compound (7b) confirmed the ROS‐independent cell death. These results demonstrate that compound (7b) could serve as a valuable template for the development of novel synthetic compounds as potential anticancer agents for hepatocellular carcinoma treatment.
Neuroprotective effect of quercetin against radiation‐induced endoplasmic reticulum stress in neurons
Authors: Chatterjee Jit , Langhnoja Jaldeep , Pillai Prakash P , Mustak Mohammed S 
Published: October 2018

AbstractThe endoplasmic reticulum (ER) plays an important role in the regulation and maintenance of cellular homeostasis. However, unresolved ER stress leads to deleterious effects by inducing the accumulation of unfolded proteins in the cell. Here we have demonstrated the protective aspects of quercetin against radiation‐induced ER stress and against inflammation in primary cultured dorsal root ganglion (DRG) neurons. The mature DRG neurons were pretreated with different concentrations of quercetin (5‐100 μM) for 24 hours before 2 Gy gamma radiation exposure and then subjected to a cytotoxicity assay, quantitative real‐time polymerase chain reaction and Western blot analysis. The results showed that quercetin decreased the expression of BiP and C/EBP‐homologous protein, the ER stress marker genes along with downregulation of tumor necrosis factor‐α, JNK in irradiated DRG neurons. Furthermore, quercetin pretreatment significantly increased the cytoskeletal protein Tuj1 and the neurotrophin brain‐derived neurotrophic factor in the neuron. These results indicate that quercetin plays a neuroprotective role against radiation‐mediated ER stress and inflammatory responses.
Boron ameliorates arsenic‐induced DNA damage, proinflammatory cytokine gene expressions, oxidant/antioxidant status, and biochemical parameters in rats
Authors: Ince Sinan , Kucukkurt Ismail , Acaroz Ulas , Arslan‐Acaroz Damla , Varol Nuray 
Published: October 2018

AbstractArsenic, an element found in nature, causes hazardous effects on living organisms. Meanwhile, natural compounds exhibit protective effects against hazardous substances. This study evaluated the effects of boron against arsenic‐induced genotoxicity and altered biochemical parameters in rats. Thirty‐five male Wistar albino rats were equally divided into five groups, and the experimental period lasted 30 days. One group was used as the control, and another group was treated with 100 mg/L arsenic in drinking water. The other groups were orally treated with 5, 10, and 20 mg/kg boron plus arsenic (100 mg/L via drinking water). Arsenic caused changes in biochemical parameters, total oxidant/antioxidant status, and DNA damage in mononuclear leukocytes. Moreover, it increased IFN‐γ, IL‐1β, TNF‐α, and NFκB mRNA expression levels in rat tissue. However, boron treatment improved arsenic‐induced alterations in biochemical parameters and increases in DNA damage and proinflammatory cytokine gene expressions.
Hesperidin promotes lysosomal biogenesis in chronically ethanol‐induced cardiotoxicity in rats: A proposed mechanisms of protection
Authors: Gaballah Hanaa H. , Ghanem Heba B. , Tahoon Nahid M. , Mohamed Darin A. , Ebeid Abla M. 
Published: October 2018

AbstractAlcohol consumption is a major global risk factor for mortality and morbidity. We aimed to delineate the mechanisms underlying the potential ameliorative effects of hesperidin against chronically ethanol‐induced cardiotoxicity. Sixty male albino rats were divided into normal control group, hesperidin‐treated control group, untreated alcoholic group, and hesperidin‐treated alcoholic group. Transcription factor‐EB (TFEB) expression levels were estimated using real‐time reverse transcription‐polymerase chain reaction. Peroxisome proliferator–activated receptor γ coactivator 1‐α (PGC1‐α), macrophage inflammatory protein‐1 α, poly‐(ADP‐ribose)‐polymerase‐1 (PARP‐1) activity, and tenascin C levels in cardiac tissues were estimated by enzyme‐linked immunosorbent assay; while tissue malondialdehyde and total antioxidant capacity were evaluated spectrophotometrically. Our data portrayed promoting lysosomal biogenesis, as judged by upregulation of TFEB expression and its target PGC1‐α, as well as decreased PARP‐1 activity and offsetting inflammation, oxidative stress, and tissue injury as the principal culprits mediating the cardioprotective effect of hesperidin in alcohol‐induced cardiotoxicity. In conclusion, hesperidin can be used as a cardioprotective agent in chronically ethanol‐induced cardiotoxicity.
Hydrogen sulfide alleviates uranium‐induced rat hepatocyte cytotoxicity via inhibiting Nox4/ROS/p38 MAPK pathway
Authors: Yi Juan , Yuan Yan , Zheng Jifang , Zhao Tingting 
Published: October 2018

AbstractAs a gasotransmitter, hydrogen sulfide (H2S) plays a crucial role in regulating the signaling pathway mediated by oxidative stress. The purpose of this study was to investigate the protective effects of H
2S on uranium‐induced rat hepatocyte cytotoxicity. Primary hepatocytes were isolated and cultured from
Sprague Dawley rat liver tissues. After pretreating with sodium hydrosulfide (an H
2S donor) for 1 hour (or GKT‐136901 for 30 minutes), hepatocytes were treated by uranyl acetate for 24 hours. Cell viability, reactive oxygen species (ROS), malondialdehyde (MDA), NADPH oxidase 4 (Nox4), and p38 mitogen‐activated protein kinase (p38 MAPK) phosphorylation were respectively determined. The effects of direct inhibition of Nox4 expression by GKT‐136901 (a Nox4 inhibitor) on ROS and phospho‐p38 MAPK levels were examined in uranium‐treated hepatocytes. The results implicate that H
2S can afford protection of rat hepatocytes against uranium‐induced adverse effects through attenuating oxidative stress via prohibiting Nox4/ROS/p38 MAPK signaling.
Investigation of the effect of telomerase inhibitor BIBR1532 on breast cancer and breast cancer stem cells
Authors: Doğan Fatma , Özateş Neslihan Pınar , Bağca Bakiye Göker , Abbaszadeh Zeka , Söğütlü Fatma , Gasımlı Röya , Gündüz Cumhur , Biray Avcı Çığır 
Published: October 2018

AbstractIt is emphasized that cancer stem cells (CSCs) forming the subpopulation of tumour cells are responsible for tumour growth, metastasis, and cancer drug resistance. Inadequate response to conventional therapy in breast cancer leads researchers to find new treatment methods and literature surveys that support CSC studies. A selective anticancer agent BIBR1532 inhibits the telomerase enzyme. Many of the chemotherapeutic drugs used in clinical trials have harmful effects, but the advantage of telomerase‐based inhibitors is that they are less toxic to healthy tissues. The phosphoinositide 3‐kinase (PI3K)/serine/threonine kinase (Akt)/mammalian target of rapamycin (mTOR) pathway is common in breast cancer, and the interaction between the mTOR pathway and human telomerase reverse transcriptase (hTERT) is essential for the survival of cancer cells. In our study, we treated MCF‐7, breast cancer stem cell (BCSC) and normal breast epithelial cell MCF10A with the BIBR1532 inhibitor. The IC
50 doses for the 48th hour of BIBR1532 treatment were detected as 34.59 μM in MCF‐7, 29.91 μM in BCSCs, and 29.07 μM in MCF10A. It has been observed that this agent induces apoptosis in the BCSC and MCF‐7 cell lines. According to the results of cell cycle analysis, G
2/M phase accumulation was observed in BCSC and MCF‐7 cell lines. It has also been shown that BIBR1532 suppresses telomerase activity in BCSC and MCF‐7. The effect of BIBR1532 on the mTOR signalling pathway has been investigated for the first time in this study. It is thought that the telomerase inhibitor may bring a new approach to the treatment and it may be useful in the treatment of CSCs.
Involvement of NYD‐SP15 in growth and oxidative‐stress responses of ARPE‐19
Authors: Xu Yidan , Wang Linnong , Cao Liu , Chen Lixun , Liu Qinghuai 
Published: October 2018

AbstractThe aim of this study was to investigate the role of NYD‐SP15 in the growth and oxidative‐stress responses of ARPE‐19 cells. ARPE‐19 cell lines overexpressing wild type or RNA interference against NYD‐SP15 were established via lentivirus transfection. Cell growth and proliferation, migration, apoptosis, and cell cycle progression were monitored using the Cell Counting Kit‐8 assay, the wound scratch assay, and flow cytometry, respectively. Caspase‐3/8/9 activity was examined using the caspase‐3/8/9 assay kit. An hydrogen peroxide (H
2O
2)–induced oxidative‐stress damage model was used to study the effect of NYD‐SP15 knockdown by examining the activity of reactive oxygen species (ROS). Expressions of Kelch‐like ECH‐associated protein 1 (Keap‐1)/heme oxygenase‐1 (HO‐1)/nuclear factor erythroid 2–related factor 2 (Nrf2), mitogen‐activated protein kinase (MAPK), and Akt were detected by Western blot analysis. The mRNA chip of NYD‐SP15 overexpressed ARPE‐19 cells as well as controls were performed by one array plus process. Overexpression (OE) of NYD‐SP15 inhibited the proliferation and migration of ARPE‐19 cells, and led to apoptosis and caspase‐3/9 activation. OE of NYD‐SP15 inhibited MAPKs and Akt signaling. Downregulation of NYD‐SP15 had no effect on the growth of normally cultured ARP19 cells with 10% fetal bovine serum, but promoted the growth of ARP19 cells in the presence of starvation challenge. Gene chip showed that OE of NYD‐SP15 led to downregulation of 254 genes and upregulation of 57 genes. Downregulation of NYD‐SP15 also exerted a protective effect on H
2O
2‐induced cell apoptosis and ROS. NYD‐SP15 downregulation led to increments in the expression of Nrf2, Keap‐1, and HO‐1 in response to 200 μM H
2O
2. NYD‐SP15 might inhibit the growth, proliferation, and migration and promote apoptosis of ARPE‐19 cells via MAPK and Akt signaling. Downregulation of NYD‐SP15 could protect ARPE‐19 cells from H
2O
2‐induced oxidative damage by active Keap‐1/HO‐1/Nrf2, Akt, and MAPK signaling.
Exploring the antidiabetic and anti‐obesity properties of Samanea saman through in vitro and in vivo approaches
Authors: Vinodhini Shanmugam , Rajeswari V. Devi 
Published: October 2018

AbstractIn recent years, diabetes and obesity have become a major problem in global health care because of changes in lifestyle, food habits, and age‐related metabolic disorders. Diabetes mellitus is one of the most common diseases, affecting millions of people worldwide. Currently, herbal drugs are used to control obesity and diabetes. The present study investigates the anti‐obesity, antidiabetic, and antioxidant activities of Samanea saman leaf extract. A methanolic extract of
S. saman leaves was prepared by a maceration method. The
S. saman leaf extract was studied for its inhibitory effect on glucose utilization using specific in vitro procedures to analyze its antioxidant, anti‐obesity, and antidiabetic activities via different assays, such as α‐amylase and α‐glucosidase inhibition assay, glucose uptake by yeast cells, nonenzymatic glycosylation assay followed by glucose diffusion assay. The outcome of the study showed that the methanolic extract strongly inhibited the pancreatic lipase, α‐amylase, and glucosidase activities, compared with the standard drug. The results showed that the extract possessed considerable antioxidant and antidiabetic activities, and further studies are needed to confirm the results using an in vivo model. Thus, it is proposed that
S. saman can be used as a therapeutic agent.
Perilaldehyde activates AMP‐activated protein kinase to suppress the growth of gastric cancer via induction of autophagy
Authors: Zhang Yu , Liu Suosi , Feng Qin , Huang Xiuyun , Wang Xiangyang , Peng Ya , Zhao Zhihong , Liu Zhan 
Published: October 2018

AbstractBackground and Aim: Perillaldehyde (PAH), one of the major oil components in
Perilla frutescens, is very critical to health maintenance, for a wide range of human chronic diseases, including cancers. AMP‐activated protein kinase (AMPK) has been implicated in the activation of autophagy in distinct tissues. This study was designed to explore whether PAH prevents gastric cancer growth and to investigate the molecular mechanism.Methods and Results: In cultured mouse gastric cancer cell line MFCs and human gastric cancer cell lines GC9811‐P, PAH activated AMPK by increasing the Thr172 phosphorylation and activity in a time‐/concentration‐dependent manner. Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3‐Methyladenine (3‐MA). In vivo studies indicated that 4‐week administration of PAH (100 mg/kg/day) suppressed the growth of gastric cancer and increased the levels of autophagy‐related proteins, including beclin‐1, LC3‐II, cathepsin, caspase‐3, p53, and cathepsin in tumors isolated from the xenograft model of gastric cancer in mice. Moreover, these anticancer effects produced by PAH were abolished by coadministration of compound C or 3‐MA in vivo.Conclusions: PAH increases AMPK phosphorylation and activity to induce gastric cancer cell autophagy to inhibit the growth of gastric cancer. In perspective, therapy of PAH should be applied to treat patients with gastric cancer.
Downregulation of antidifferentiation noncoding RNA promotes chondrogenic differentiation and calcification of ligamentum flavum‐derived mesenchymal stem cells
Authors: Zhang Qiang , Wang Shenyu , Sheng Yifei , Zhao Shujie , Jiang Yuqing , Zhou Dong , Yang Huilin 
Published: October 2018

AbstractLigamentum flavum (LF)‐derived mesenchymal stem cells (MSCs) have been implicated in the pathogenesis of calcification of the ligamentum flavum (CLF) leading to the increased presence of chondrocyte‐like cells and calcium deposition in CLF; however, the mechanisms of LF‐MSCs in differentiation are not defined. In this study, we investigated the role of antidifferentiation noncoding RNA (ANCR) in the differentiation of LF‐MSCs. We found that ANCR was downregulated in human CLF tissues. In cultured LF‐MSCs, ANCR downregulation led to decreased cell proliferation but enhanced chondrogenic differentiation and calcification. In contract, ANCR overexpression increased cell proliferation but inhibited differentiation and calcification. Mechanistically, we detected a positive correlation between ANCR and enhancer of zeste homolog 2 (EZH2) in human CLF tissues. In cultured LF‐MSCs, ANCR knockdown decreased while ANCR overexpression increased EZH2 expression. In addition, physical association between ANCR and EZH2 was revealed by an RNA pull‐down assay. Functionally, EZH2 overexpression prevented chondrogenic differentiation and calcification enhanced by ANCR knockdown. These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF‐MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte‐like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF.