bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modelling farmers' responses to irrigation water policies in Algeria: An economic assessment of volumetric irrigation prices and quotas in the Jijel–Taher irrigated perimeter
Authors: Oulmane Amine , Frija Aymen , Brabez Fatima 
Published: February 2019

AbstractIn Algeria, the management of water based on a strategy of supply and subsidies continues to be applied even as the resource becomes increasingly scarce. The demand for water in Algeria continues to grow, creating an imbalance between the available water resources and uses. In this context, the state has progressively implemented irrigation water management policies, including pricing, which aims to manage demand while reducing the water price subsidy. In this article we will study the effectiveness of some water management instruments implemented in the large irrigation perimeters and offer some perspectives to improve the management of the demand for irrigation water. To do so, we investigate the effect of different water pricing and irrigation quota scenarios on changing farmers' behaviour in terms of irrigation water demand. We developed a positive mathematical programming model based on farmers' surveys and typology in a public irrigated scheme (Jijel–Taher located in northern Algeria). Two types of scenarios were simulated, including: (i) increasing volumetric prices of irrigation water in the studied irrigated areas; (ii) decreasing water quota scenarios allocated to the farmers. As expected, results show that increasing water prices may lead to a decreasing demand for irrigation water. However, this decrease in water demand only became significant at very high prices. We also found that a price of 12.5 DZD m‾3 (about 0.11 US$ m‾3), corresponding to the government production cost of water, can easily be implemented in the study area without substantial effects on farmers' gross margin. Then, water pricing does not represent a water demand management tool, but rather a tool to finance management infrastructures. Simulations also show that decreasing water quotas may lead to a decrease of irrigated areas, change in cropping patterns, and to a significant loss of farmers' gross margins for quotas below 2600 m3 ha‾¹. © 2019 John Wiley & Sons, Ltd.
Genetic association of DNMT variants can play a critical role in defining the methylation patterns in autism
Authors: Alex Ann Mary , Saradalekshmi Korammannil R. , Shilen Neena , Suresh Poovathinal A. , Banerjee Moinak 
Published: February 2019

ABSTRACTAutism spectrum disorder (ASD) is a complex neurodevelopmental disorder with impairments in social communication, restricted, repetitive and stereotyped behaviors. Both genetic and environmental factors are known to contribute toward pathophysiology of Autism. Environmental influences on gene expression can be mediated by methylation patterns which are established and maintained by DNA methyltransferases. Several studies in the past have investigated the role of global methylations in Autism. The present study is aimed to investigate the role of genetic variations in the DNA methyltransferase which might be critical in defining the threshold for environmental factors toward susceptibility to autism. Polymorphisms in DNA methyltransferases, DNMT1, DNMT3A, DNMT3B, and DNMT3L were screened for association with ASD in 180 autistic patients and 260 healthy controls from a south Indian population. DNMT1 rs10418707 and rs10423341, and DNMT3A rs2289195 were found to be significantly associated at genotypic and allelic level with ASD. Functional prediction indicates that these SNPs have a role in transcriptional regulation and increased expression, indicating that hypermethylation might be induced by its genotype status. The study might reflect the role of genetics variants in DNMTs in defining the threshold of environmental impact in influencing the disease or phenotype variations in ASD. © 2019 IUBMB Life, 2019
Cytotoxicity profile of pristine graphene on brain microvascular endothelial cells
Authors: Rosas‐Hernandez Hector , Escudero‐Lourdes Claudia , Ramirez‐Lee Manuel A. , Cuevas Elvis , Lantz Susan M. , Imam Syed Z. , Majeed Waqar , Bourdo Shawn E. , Paule Merle G. , Biris Alexandru S. , Ali Syed F. 
Published: February 2019

AbstractGraphene‐based nanomaterials hold the potential to be used in a wide variety of applications, including biomedical devices. Pristine graphene (PG) is an un‐functionalized, defect‐free type of graphene that could be used as a material for neural interfacing. However, the neurotoxic effects of PG, particularly to the blood‐brain barrier (BBB), have not been fully studied. The BBB separates the brain tissue from the circulating substances in the blood and is essential to maintain the brain homeostasis. The principal components of the BBB are brain microvascular endothelial cells (BMVECs), which maintain a protectively low permeability due to the expression of tight junction proteins. Here we analyzed the effects of PG on BMVECs in an in vitro model of the BBB. BMVECs were treated with PG at 0, 10, 50 and 100 μg/mL for 24 hours and viability and functional analyses of BBB integrity were performed. PG increased lactate dehydrogenase release at 50 and 100 μg/mL, suggesting the induction of necrosis. Surprisingly, 2,3,‐bis(2‐methoxy‐4‐nitro‐5‐sulfophenyl)‐5‐[(phenylamino)‐carbonyl]‐2H‐tetrazolium (XTT) conversion was increased at 10 and 50 μg/mL. In contrast, XTT conversion was decreased at 100 μg/mL, suggesting the induction of cell death. In addition, 100 μg/mL PG increased DNA fragmentation, suggesting induction of apoptosis. At the same time, 50 and 100 μg/mL of PG increased the endothelial permeability, which corresponded with a decrease in the expression of the tight junction protein occludin at 100 μg/mL. In conclusion, these results suggest that PG negatively affects the viability and function of the BBB endothelial cells in vitro.
Current state‐of‐the‐art and future perspectives of the three main modern implant‐dentistry concerns: Aesthetic requirements, mechanical properties, and peri‐implantitis prevention
Authors: López‐Píriz Roberto , Cabal Belén , Goyos‐Ball Lidia , Fernández Adolfo , Bartolomé José F. , Moya Jose S. , Torrecillas Ramón 
Published: February 2019

AbstractThe idea of permanent tooth replacement goes back to the year 2000 BC at least, when carved bamboo pegs were used to replace missing teeth in ancient China. The phenomenon of osseointegration, however, was not verified until the mid‐1960s, when Branemark discovered that titanium could integrate to bone. Since then, the osseointegration capacity of implants has been profoundly investigated and implants as such have evolved enormously in all possible aspects, from material selection and processing to specific surface engineering, among many others. This review article, in particular, focuses on dental implants and aims to introduce the main concerns involved in modern dentistry, concentrating especially on the importance of finding an effective way to prevent peri‐implantitis. In this sense, strategies such as shifting from metal to ceramic implant components and applying novel antimicrobial antibiotic‐free coatings seem to be taking the lead. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2019.
Simple fabrication of inner chitosan‐coated alginate hollow microfiber with higher stability
Authors: Liu Hui , Wang Yaqing , Yu Yue , Chen Wenwen , Jiang Lei , Qin Jianhua 
Published: February 2019

AbstractSodium alginate (NaA) has been widely used as microfiber‐based scaffold material. However, Ca‐alginate microfiber might disintegrate in the physiological environment due to the loss of calcium ions, which will limit its long‐term application in tissue engineering. In this work, to enhance the stability of Ca‐alginate microfiber in the physiological environment, an inner chitosan coating was introduced to Ca‐alginate hollow microfiber by one step via a microfluidic device. A more stable composite microfiber with double cross‐linking layers was generated. The stability of the microfiber was studied in the PBS solution (pH 7.4) to identify the coating effect on the hollow structure. The results revealed that chitosan component bonded an NaA layer to form a stable polyelectrolyte complex membrane in the inner wall of the microfiber, which stabilized the hollow region even though the Ca‐alginate shell was disintegrated by PBS solution. In addition, the introduction of chitosan coating improved the inner environment of the low affinity of alginate to cell surfaces and facilitated the cell adhesion and culture in the microfiber. HepG2 cells in the microfibers displayed favorable cell viability and proliferation ability. We believe that this work will lead to the development of innovative methodologies and materials for both cell culture and tissue engineering application. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B:2527–2536, 2019.
Combination Therapy With Zoledronic Acid and FES‐Row Training Mitigates Bone Loss in Paralyzed Legs: Results of a Randomized Comparative Clinical Trial
Authors: Morse L R , Troy K L , Fang Y , Nguyen N , Battaglino R , Goldstein R F , Gupta R , Taylor J A 
Published: February 2019

AbstractSpinal cord injury (SCI) results in rapid, severe osteoporosis and an increased risk of lower extremity fractures. Despite the medical complications associated with these fractures, there is no standard of care to prevent osteoporotic fractures following SCI. Functional electrical stimulation‐ (FES‐) assisted rowing is a promising intervention to improve bone health in SCI because of its ability to generate a muscular contraction in conjunction with mechanical loading of the lower extremity long bones. Combination therapy consisting of FES‐rowing plus zoledronic acid (ZA) may be a superior treatment via inhibition of bone resorption and stimulation of new bone formation. We studied participants enrolled in a randomized clinical trial comparing FES‐rowing alone with FES‐rowing plus ZA to improve bone health in SCI. Volumetric CT scans at the distal femur and proximal tibial metaphyses were performed. Bone geometric properties (cortical thickness index [CTI], cortical compressive strength index [CSI], buckling ratio [BR], bending strength index) and mineral (cortical bone volume [CBV], cortical bone mineral density, cortical bone mineral content) indices were determined. In models adjusting for baseline values, we found that the CBV (p = 0.05 to 0.006), the CTI (p = 0.009), and the BR (p = 0.001) at both the distal femoral and proximal tibial metaphyses were greater in the ZA plus rowing group compared with the rowing‐only group. Similarly, there was a significant positive association between the total rowing work completed and the BR at the proximal tibia (p = 0.05). A subgroup analysis of the rowing‐only arm showed that gains in the CSI at the tibial metaphysis varied in a dose‐dependent fashion based on the total amount of exercise performed (p = 0.009). These findings demonstrate that the osteogenic response to FES‐rowing is dose‐dependent. Combination therapy with ZA and FES‐row training has therapeutic potential to improve bone quality, and perhaps reduce fracture risk at the most common fracture site following SCI. © 2019 The Authors. JBMR Plus Published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
Maternal Transient Receptor Potential Vanilloid 6 (Trpv6) Is Involved In Offspring Bone Development
Authors: Fecher-Trost Claudia , Lux Femke , Busch Kai-Markus , Raza Ahsan , Winter Manuel , Hielscher Franziska , Belkacemi Thabet , van der Eerden Bram , Boehm Ulrich , Freichel Marc , Weissgerber Petra 
Published: February 2019

ABSTRACT

Embryonic growth and bone development depend on placental Ca2+ transport across the feto-maternal barrier to supply minerals to the fetus. The individual factors and cellular mechanisms that regulate placental Ca2+ transfer, however, are only beginning to emerge. We find that the Ca2+-selective transient receptor potential vanilloid 6 (TRPV6) channel is expressed in trophoblasts of the fetal labyrinth, in the yolk sac, and in the maternal part of the placenta. Lack of functional TRPV6 channels in the mother leads to a reduced Ca2+ content in both placenta and embryo. Ca2+ uptake in trophoblasts is impaired in the absence of Trpv6. Trpv6-deficient embryos are smaller, have a lower body weight, and shorter and less calcified femurs. The altered cortical bone microarchitecture persists in adulthood. We show that TRPV6's Ca2+-conducting property causes this embryonic and bone phenotype. Our results show that TRPV6 is necessary for the Ca2+ uptake in trophoblasts and that TRPV6 deficiency in the placenta leads to reduced embryo growth, minor bone calcification, and impaired bone development. © 2019 American Society for Bone and Mineral Research.
A comprehensive analysis of WGCNA and serum metabolomics manifests the lung cancer‐associated disordered glucose metabolism
Authors: Ding Mingchao , Li Fang , Wang Bin , Chi Guoqing , Liu Hao 
Published: February 2019

AbstractLung cancer is a worldwide disease and highly heterogeneous at a molecular level. In this study, we both performed the pathway enrichment analysis and the transcriptome‐based weighted gene coexpression network analysis (WGCNA) so as to find the critical pathways involved in lung cancer. Our analysis results indicated that genes in viability modules (0 < Z‐summary < 2) selected by WGCNA were more reliable for identifying crucial pathways, while gene enrichment analysis provided a wide range of pathways with a little emphasis on target pathways for lung cancer. On the basis of genes, which were classified into various modules by WGCNA, we found a significant aberration of glucose metabolism in lung cancer cells, demonstrating that the glucose metabolism has been perturbed, especially the glycolysis pathway. Our study revealed that disordered glucose metabolism might be closely associated with the carcinogenesis of lung cancer based on the integrated analysis of WGCNA and metabolomics, which could be a potential therapeutic target for lung cancer.
Sirtuin 6 mitigated LPS‐induced human umbilical vein endothelial cells inflammatory responses through modulating nuclear factor erythroid 2‐related factor 2
Authors: Qin Yi , Cao Lirong , Hu Lili 
Published: February 2019

AbstractBackgroundNuclear factor erythroid 2‐related factor 2 (Nrf2) protects the lung from sepsis‐induced injury through activating Nrf2‐regulated multiple phase 2 detoxification genes, including NAD(P)H: quinine oxidoreductase‐1 (NQO1) and heme oxygenase‐1 (HO1). Based on the positive effect of Sirtuin 6 on Nrf2, we aim to explore the potential role of SIRT6 in the mechanism of sepsis‐induced acute lung injury (ALI).MethodsMouse models of sepsis were constructed by instilling intratracheal of lipopolysaccharide (LPS; 4 ml/kg). After 48‐hour treatment, lung tissues were collected to measure the degree of lung injury. The SIRT6, siSIRT6, and siNrf2 plasmids were cotransfected into various concentrations of LPS‐treated human umbilical vein endothelial cells (HUVECs; 0, 1, 5, 10, and 50 μg/ml) using Lipofectamine 2000. Tumor necrosis factor‐α (TNF‐α) and interleukin (IL)‐6 levels were determined by enzyme‐linked immunosorbent assay. Expression levels of SIRT6, Nrf2, NQO1, and HO1 was measured by quantitative polymerase chain reaction and Western blot analysis. Cell apoptosis was determined by flow cytometry.ResultsLung tissues in the model group already had basic characteristics of ALI. Compared with the control model, TNF‐α and IL‐6 levels were much higher (P < 0.01), the levels of SIRT6, Nrf2, and Nrf2‐modulated detoxification factors were downregulated (P < 0.01). SIRT6 overexpression decreased the apoptosis below to 10% (P < 0.01), significantly increased the Nrf2 expression, effectively inhibited TNF‐α and IL‐6 releases, and enhanced NQO1 and HO1 levels (P < 0.01). siNrf2 abolished the protective effects of SIRT6 overexpression, including increasing apoptosis and inhibiting anti‐inflammatory and antioxidative genes expressions (P < 0.01).ConclusionsOur study suggested SIRT6 positively regulated Nrf2 expression and activated Nrf2‐regulated anti‐inflammatory and antioxidative enzymes, which could effectively mitigate LPS‐induced HUVECs inflammatory responses. This might reflect the mechanism of ALI induced by sepsis.
Biological features and regulatory mechanisms of salt tolerance in plants
Authors: Li Jingrui , Liu Min 
Published: February 2019

AbstractHalophytes play a vital role in saline agriculture because these plants are necessary to increase the food supply to meet the demands of the growing world population. In addition, the transfer of salt‐resistance genes from halophytes using genetic technologies has the potential to increase the salt tolerance of xerophytes. Characterization of some particularly promising halophyte model organisms has revealed the important new insights into the salt tolerance mechanisms used by plants. Numerous advances using these model systems have improved our understanding of salt tolerance regulation and salt tolerance‐associated changes in gene expression, and these mechanisms have important implications for saline agriculture. Recent findings provide a basis for future studies of salt tolerance in plants, as well as the development of improved strategies for saline agriculture to increase yields of food, feed, and fuel crops.
Regulation of P300 and HDAC1 on endoplasmic reticulum stress in isoniazid‐induced HL‐7702 hepatocyte injury
Authors: Li Jin‐Feng , Li Ying‐Shu , Zhang Yi‐Yang , Sun Shu‐Feng , Han Tie‐Sheng , Li Yu‐Hong , Feng Fu‐Min 
Published: February 2019

AbstractP300 and HDAC1 can be involved in the development of various liver diseases by regulating gene transcription. Endoplasmic reticulum stress (ERS) is one of the main pathways of apoptosis and is activated during inflammatory responses, but the roles of P300 and HDAC1 in ERS in antituberculosis drug‐induced liver injury (ADLI) are not clear. This study confirms that isoniazid can change the states of P300 and HDAC1 in HL‐7702 hepatocyte metabolism and induce ERS, causing hepatocyte injury and apoptosis. When combined with C646, however, P300 can be reduced. HL‐7702 cells were flattened, and the cytoplasm became crinkled. To a certain extent, ERS was relieved, but hepatocytes suffered worse damage, and the rate of cell apoptosis markedly increased. When MS‐275 was applied, HDAC1 level was increased, cell fusion appeared, and fluorescence intensity of endoplasmic reticulum was weakened. In addition, ERS was aggravated, but liver injury was relieved, and the apoptosis rate significantly decreased. Therefore, alteration of P300 and HDAC1 status and ERS are involved in ADLI, and changes in P300 and HDAC1 can regulate ERS and then affect cell damage.
Current information on the association of Helicobacter pylori with autophagy and gastric cancer
Authors: Eslami Majid , Yousefi Bahman , kokhaei Parviz , arabkari Vahid , Ghasemian Abdolmajid 
Published: February 2019

AbstractHelicobacter pylori (H. pylori) is a Gram‐negative bacterium and causative agent of gastric cancer. H. pylori induce defective autophagy or inhibit it by means of CagA and vacuolating cytotoxin A (VacA) toxins leading to the gastric cancer induction. Impaired or defective autophagy leads to the accumulation of cytotoxic materials, such as ROS and P62 that lead to increased mutations in the DNA, genome instability, and risk of cancer formation. H. pylori CagA may inhibit autophagy through the c‐Met‐PI3k/Akt‐mTOR signaling pathway. However, VacA induces autophagy by some signaling pathways. In the gastric epithelial cells, VacA is a necessary and sufficient factor for the creation of autophagy. While CagA is a negative regulator of this phenomenon, the elimination of this gene from H. pylori has increased autophagy and the production of inflammatory cytokines is reduced. In gastrointestinal cancers, some of the microRNAs (miRNAs) act as tumor suppressors and some other are oncogenes by regulating various genes expression. H. pylori can also modify autophagy through a mechanism that includes the function of miRNAs. In autophagy, oncogenic miRNAs inhibit activation of some tumor suppressor signaling pathways (e.g., ULK1 complex, Beclin‐1 function, and Atg4 messaging), whereas tumor suppressor miRNAs can block the activation of oncogenic signaling pathways. For instance, Beclin‐1 is negatively regulated by miRNA‐376b (oncogenic miRNA) and miRNA‐30a (tumor suppressor miRNA). Similarly, Atg4 by miRNA‐376b (oncogenic miRNA) and miRNA‐101 (tumor suppressor miRNA). So, this apparent paradox can be explained as that both Beclin‐1 and Atg4 play different roles in a particular cell or tissue.
Is it true that gut microbiota is considered as panacea in cancer therapy?
Authors: Salek Farrokhi Amir , Darabi Narges , Yousefi Bahman , Askandar Rafee Habib , Shariati Mansoreh , Eslami Majid 
Published: February 2019

AbstractRecent studies demonstrated that a combination of the gut microbiome has the vital effect on the efficacy of anticancer immune therapies. Regulatory effects of microbiota have been shown in different types of cancer therapies such as chemotherapy and immunotherapy. Immune‐checkpoint‐blocked therapies are the recent efficient cancer immunotherapy strategies. The target of immune‐checkpoint blocking is cytotoxic T lymphocyte protein‐4 (CTLA‐4) or blockade of programmed death‐1 (PD‐1) protein and its ligand programmed death ligand 1 (PD‐L1) that they have been considered as cancer immunotherapy in recent years. In the latest studies, it have been demonstrated that several gut bacteria such as Akkermansia muciniphila,
Bifidobacterium spp.,
Faecalibacterium spp., and
Bacteroides fragilis have the regulatory effects on PD‐1, PD‐L1, and CTLA‐4 blocked anticancer therapy outcome.
Combinatorial effect of blueberry extracts and oxaliplatin in human colon cancer cells
Authors: Lin Yang , Li Bin , Zhao Jin , Wei Lulu , Wang Yuehua , Wang Mingyue , Dia Vermont P. , Meng Xianjun 
Published: February 2019

AbstractThe use of natural compounds to potentiate the effect of drugs and lower their adverse effects is an active area of research. The objective is to determine the effect of combined blueberry extracts (BE) and oxaliplatin (OX) in colon cancer cells. The results demonstrated that treatments of BE/OX showed inhibitory effects on HCT‐116 cell and nontoxic effect on CCD‐18Co normal colon cells. Flow cytometry analysis indicated that treatment with the BE, OX or in combination could induce G0/G1 cell cycle arrest, apoptosis, increase of reactive oxygen species, and induce loss of mitochondrial membrane potential in HCT‐116 cells. Furthermore, after treatments, the expression of inflammatory cytokines was decreased, cyclin D1 and CDK4 were decreased; caspases‐3 and 9 were activated; the Akt/Bad/Bcl‐2 pathway was modulated. Moreover, the combination treatment had a considerably higher growth inhibitory effect on human colon cancer HCT‐116 cells than that of BE or oxaliplatin alone. Our results showed that BE increased the anticolon cancer effect of OX making it an attractive strategy as adjuvant therapy to potentially reduce the adverse side effects associated with chemotherapeutic drugs.