bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reinforcement learning algorithm for 5G indoor device‐to‐device communications
Authors: Sreedevi A.G. , Rama Rao T. 
Published: June 2019

AbstractFifth generation (5G), the next generation telecommunications will be striking the markets in near future. Device‐to‐device (D2D) communication would be a part of 5G to serve communication needs for billions of connected devices to support high data rate ultrareliable low latency communications. Indoor 5G will be relying on distributed small cell solutions and D2D along with machine‐to‐machine connections. Machine learning is one of the most promising tools for providing the best set of solutions to learn the influential scenarios and certain parameters of the communication networks. This research proposes reinforcement‐learning‐based latency controlled D2D connectivity (RL‐LCDC) algorithm and its Q‐learning approach in an indoor D2D communication network for strong 5G connectivity with minimum latency. The proposed approach, RL‐LCDC efficiently discovers the neighbors, decides the D2D link, and adaptively controls the communication range for maximum network connectivity. The results show that RL‐LCDC optimizes the connectivity with lower end‐to‐end delay and better energy efficiency with efficient convergence time when compared with other conventional schemes.
Fully coupled free‐surface flow and sediment transport modelling of flash floods in a desert stream in the Mojave Desert, California
Authors: Khosronejad Ali , Kang Seokkoo , Flora Kevin 
Published: June 2019

AbstractFor most of the year, a dry‐bed desert wash is void of water flow. Intensive rain events, however, could trigger significant flash floods that bring about highly complicated hydrodynamics and morphodynamics processes within a desert stream. We present a fully coupled three‐phase flow model of air, water, and sediment to simulate numerically the propagation of a flash flood in a field‐scale fluvial desert stream, the so‐called Tex Wash located in the Mojave Desert, California, United States. The turbulent flow of the flash flood is computed using the three‐dimensional unsteady Reynolds‐averaged Navier–Stokes equations closed with the shear stress transport k − ω model. The free surface of the flash flood at the interface of air and water phases is computed with the level‐set method, which enables instantaneous tracking of the water surface as the flash flood propagates over the dry bed of the desert stream. The evolution of the desert fluvial stream's morphology, due to the action of the propagating flash flood on the mobile bed, is calculated using a Eulerian morphodynamics model based on the curvilinear immersed boundary method. The capabilities of the proposed numerical framework are demonstrated by applying it to simulate a flash flood event in a 0.65‐km‐long reach of the Tex Wash, the intricate channel morphology of which is obtained using light imaging detection and ranging technology. The simulated region of the stream includes a number of bridge foundations. The simulation results of the model for the flash flood event revealed the formation of a highly complex flow field and scour patterns within the stream. Moreover, our simulation results showed that most scour processes take place during the steady phase of the flash flood, that is, after the flash flood fills the stream. The transient phase of the flash flood is rather short and contributes to a very limited amount of erosion within the desert stream.
Estimation of the Value of Aquatic Ecosystem Services in the Coastal Area of Jiangsu Province, China
Authors: Yao Hong , Liu Huan , Ni Tianhua 
Published: June 2019

Abstract
Aquatic ecosystems contribute to human welfare in complex nonmarketed ways. The value of aquatic ecological services was estimated in the coastal area of Jiangsu Province, China. We used the contingent valuation method (CVM) values, including the willingness-to-pay (WTP) of households for water quality improvement and the willingness-to-accept (WTA) compensation of households for freshwater deterioration. Valid questionnaires (n = 10 814) were collected in all towns of the area (n = 367). The WTA/WTP ratios ranged from 1 to 200, the average of which was 17.7 and the median was 7.5. A multivariate linear logarithmic model was introduced to characterize the influence of demographic variables on WTP and WTA values. Residents' age, years of residency, education levels, and environmental awareness positively affected the WTA/WTP ratios. The summing of the values of aquatic ecological services in each town was ¥9.4 billion. This estimation may represent the minimum value for aquatic ecosystem services in the study area; nevertheless, this study illustrates how experience, personal wealth, and environmental awareness may influence perceptions of the value of environmental benefits and may influence policy decisions.
In vitro toxicity screening of magnetite nanoparticles by applying mesenchymal stem cells derived from human umbilical cord lining
Authors: Coccini Teresa , De Simone Uliana , Roccio Marianna , Croce Stefania , Lenta Elisa , Zecca Marco , Spinillo Arsenio , Avanzini Maria Antonietta 
Published: June 2019

AbstractDespite the growing interest in nanoparticles (NPs), their toxicity has not yet been defined and the development of new strategies and predictive models are required. Human stem cells (SCs) offer a promising and innovative cell‐based model. Among SCs, mesenchymal SCs (MSCs) derived from cord lining membrane (CL) may represent a new species‐specific tool for establishing efficient platforms for primary screening and toxicity/safety testing of NPs. Superparamagnetic iron oxide NPs, including magnetite (Fe3O4NPs), have aroused great public health and scientific concerns despite their extensive uses. In this study, CL‐MSCs were characterized and applied for in vitro toxicity screening of Fe3O4NPs. Cytotoxicity, internalization/uptake, differentiation and proliferative capacity were evaluated after exposure to different Fe3O4NP concentrations. Data were compared with those obtained from bone marrow (BM)‐MSCs. We observed, at early passages (P3), that: (1) cytotoxicity occurred at 10 μg/mL in CL‐MSCs and 100 μg/mL in BM‐MSCs (no differences in toxicity, between CL‐ and BM‐MSCs, were observed at higher dosage, 100‐300 μg/mL); (2) cell density decrease and monolayer features loss were affected at ≥50 μg/mL in CL‐MSCs only; and (3) NP uptake was concentration‐dependent in both MSCs. After 100 μg/mL Fe3O4NP exposures, the capacity of proliferation was decreased (P5‐P9) in CL‐MSCs without morphology alteration. Moreover, a progressive decrease of intracellular Fe3O4NPs was observed over culture time. Antigen surface expression and multilineage differentiation were not influenced. These findings suggest that CL‐MSCs could be used as a reliable cell‐based model for Fe3O4NP toxicity screening evaluation and support the use of this approach for improving the confidence degree on the safety of NPs to predict health outcomes.
Impaired Gastric Hormone Regulation of Osteoblasts and Lysyl Oxidase Drives Bone Disease in Diabetes Mellitus
Authors: Daley Eileen J , Pajevic Paola Divieti , Roy Sayon , Trackman Philip C 
Published: June 2019

ABSTRACTDiabetic bone disease is a complication of type I and type II diabetes, both of which are increasing in the United States and elsewhere. Increased hip and foot fracture rates do not correlate well with changes in bone mineral density (BMD), whereas studies support the importance of collagen structure to bone strength. Extracellular lysyl oxidase (LOX) catalyzes the oxidative deamination of hydroxylysine and lysine residues in collagens resulting in aldehydes that subsequently form critically important biosynthetic crosslinks that stabilize functional collagens. Although LOX‐dependent biosynthetic crosslinks in bone collagen are deficient in diabetic bone, the expression and regulation of bone LOXs in diabetes have not been comprehensively studied. Here, we found that LOX is profoundly downregulated in bone in diabetes. Moreover, we have identified a novel metabolic regulatory relationship that is dysregulated in diabetes using mouse models. Data indicate that the incretin (gastric hormone) known as glucose‐dependent insulinotropic polypeptide (GIP) that is anabolic to osteoblasts strongly upregulates LOX, and that this regulation is disrupted in the streptozotocin‐induced model of diabetes in mice. In vivo and in vitro studies support that diabetes results in elevated circulating peripheral dopamine, likely also derived from the gut, and is responsible for blocking GIP signaling and LOX levels in osteoblasts. Moreover, peripheral administration of the dopamine D2 receptor antagonist amisulpride to diabetic mice restored trabecular bone structure to near normal and partially reversed downregulation of LOX. Taken together our data identifies a novel metabolic relationship between the gut‐derived hormone GIP and bone‐derived LOX, and points to the importance of LOX dysregulation in the pathology of diabetic bone disease. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
Association of Bone Density Monitoring in Routine Clinical Practice With Anti-Osteoporosis Medication Use and Incident Fractures: A Matched Cohort Study
Authors: Leslie William D , Morin Suzanne N , Martineau Patrick , Bryanton Mark , Lix Lisa M 
Published: June 2019

ABSTRACT
Routine bone mineral density (BMD) monitoring of individuals during the initial 5 years of anti-osteoporosis treatment is controversial. Using a registry-based cohort from the Province of Manitoba, Canada, we compared anti-osteoporosis medication use and fracture outcomes in women with versus without BMD monitoring receiving anti-osteoporosis medication. We identified 4559 women aged 40 years and older receiving anti-osteoporosis therapy with serial BMD testing (monitoring) within 5 years (mean interval 3.2 years) and 4559 propensity score–matched women without BMD monitoring. We assessed anti-osteoporosis medication use over 5 years from a population-based retail pharmacy database. Incident fractures to 10 years from health services data. During median 10 years observation, 1225 (13.4%) women developed major osteoporotic fracture, including 382 (4.2%) with hip fractures. Monitored women had significantly better fracture-free survival for major osteoporotic fracture (p = 0.040; 10-year cumulative risk 1.9% lower, 95% confidence interval [CI] 0.3–3.6%) and hip fracture ( p = 0.001; 10-year cumulative risk 1.8% lower, 95% CI 0.7–2.8%) compared with women who were not monitored. Hazard ratios (HRs) were significantly lower in monitored versus not monitored women for major osteoporotic fracture (HR = 0.89, 95% CI 0.80–0.98) and hip fracture (HR = 0.74, 95% CI 0.63–0.87). Days of medication use, medication persistence ratio, and treatment switching over 5 years were greater in monitored versus not monitored women. At the end of 5 years, more women in the monitored group persisted on treatment and more switched treatment, with switching behavior associated with an observed interval reduction in BMD. In conclusion, our findings suggest a possible role for BMD monitoring after initiating anti-osteoporosis therapy in the routine clinical practice setting. © 2019 American Society for Bone and Mineral Research.
AgsA response to cadmium and copper effects at different temperatures in Escherichia coli
Authors: Lv Yanchun , Ezemaduka Anastasia N. , Wang Yunbiao , Xu Jingbo , Li Xiujun 
Published: June 2019

AbstractSmall heat shock proteins (sHsps), present from prokaryotes to eukaryotes, are a highly conserved molecular chaperone family. They play a crucial role in protecting organisms against cellular insults from single or multiple environmental stressors including heavy metal exposure, heat or cold shock, oxidative stress, desiccation, etc. Here, the toxicity of cadmium and copper, and their ability to modify the cellular growth rate at different temperatures in Escherichia coli cells were tested. Also, the response mechanism of the sHSP aggregation‐suppressing protein (AgsA) in such multiple stress conditions was investigated. The results showed that the half effect concentration (EC50) of cadmium in AgsA‐transformed E. coli cells at 37°C, 42°C, and 50°C were 11.106, 29.50, and 4.35 mg/L, respectively, and that of the control cells lacking AgsA were 5.05, 0.93, and 0.18 mg/L, respectively, while the half effect concentration (EC50) of copper in AgsA‐transformed E. coli cells at 37°C, 42°C, and 50°C were 27.3, 3.40, and 1.28 mg/L, respectively, and that of the control cells lacking AgsA were 27.7, 5.93, and 0.134 mg/L, respectively. The toxicities of cadmium and copper at different temperatures as observed by their modification of the cellular growth rate and inhibitory effects were in a dose‐dependent manner. Additionally, biochemical characterization of AgsA protein in cells subjected to cadmium and copper stresses at different temperatures implicated suppressed aggregation of cellular proteins in AgsA‐transformed E. coli cells. Altogether, our data implicate the AgsA protein as a sensitive protein‐based biomarker for metal‐induced toxicity monitoring.
Long noncoding RNA MEG3 plays a promoting role in the proliferation, invasion, and angiogenesis of lung adenocarcinoma cells through the AKT pathway
Authors: Li Hui , Wang Jue , Lv Shuang , Zhang Ying , Zhang Cuiying , Lige Baya , Dan Su , Sun Yanyan 
Published: June 2019

AbstractThe role of long noncoding RNA maternally expressed gene 3 (MEG3) in lung adenocarcinoma has not been explored entirely. In this study, it was demonstrated that the expression of MEG3 was enhanced in lung adenocarcinoma tissues from TCGA database and some specific cell lines, while the survival analysis showed that patients with higher MEG3 levels had lower survival probabilities, which suggested that MEG3 might serve as a lung adenocarcinoma promoter. In addition, the results suggested that the overexpression of MEG3 could promote the proliferation and invasion of lung adenocarcinoma cells. Furthermore, increased MEG3 expression could result in a notable increase in angiogenesis‐related factors as well as in the capillary tube formation of endothelial cells, which indicates that the overexpression of MEG3 could promote the angiogenesis of lung adenocarcinoma. From a mechanistic perspective, the results obtained revealed that the upregulation of MEG3 could stimulate the AKT signaling pathway and consequently lead to the biological behaviors mentioned above. In summary, all the results obtained from this study indicated that MEG3 plays a promoting role in the tumorigenesis and angiogenesis of lung adenocarcinoma, which deserves special attention when considered as a potential therapeutic target for lung adenocarcinoma.
DNA hypomethylation promotes invasion and metastasis of gastric cancer cells by regulating the binding of SP1 to the CDCA3 promoter
Authors: Yu Jiawei , Hua Ruheng , Zhang Yan , Tao Ran , Wang Quhui , Ni Qingfeng 
Published: June 2019

AbstractBackgroundCell division cycle associated protein‐3 (CDCA3) has been reported frequently upregulated in various cancers. It has been progressively realized that changed DNA methylations occur in diverse carcinomas. However, the concrete involvement of CDCA3 and DNA methylation in gastric cancer (GC) still needs to be further elucidated.MethodsIn this study, quantitative reverse‐transcription polymerase chain reaction (PCR) was utilized to determine the relative expressions of CDCA3 in GC and normal tissue samples. The methylation condition of CDCA3 was determined by bisulfite‐sequencing PCR (BSP) and methylation‐specific PCR (MSP). A chromatin immunoprecipitation (ChIP) assay and luciferase activity assay was used for the interaction between transcription factors and promoters and binding site determination, respectively. The effects of knockdown or overexpression of specificity protein 1 (SP1) or CDCA3 on GC cells in vitro were further assessed via wound healing assay, colony formation assay, and matrigel invasion assay.ResultsIn comparison to paired normal tissues, CDCA3 expressions were significantly increased in the GC tissues. The CDCA3 expression was regulated by DNA methylation, with the CpG island hypomethylation responsible for CDCA3 upregulation of GC. ChIP assays verified that the activity of SP1 binding to the CDCA3 promoter was dramatically increased. When the CDCA3 expression was downregulated in MKN45 cells by knockdown SP1, the proliferation ability, healing ability, and invasive ability were significantly suppressed.ConclusionThe process by which SP1 bound to the nearest promoter region was expedited in GC cells, by which DNA was hypomethylated and CDCA3 expression was promoted. The effect on cell proliferation and invasion by CDCA3 was under the regulation of SP1 and also affected by hypomethylation of DNA.
High‐mobility group box 2 promoted proliferation of cervical cancer cells by activating AKT signaling pathway
Authors: Zhang Pengnan , Lu Yuan , Gao Shujun 
Published: June 2019

AbstractCervical cancer is one of the leading killers for female worldwide. Nevertheless, the less knowledge of molecular mechanism for cervical cancer limited the improvement of treatment effects. High‐mobility group box 2 (HMGB2) belongs to the HMGB family, which could play diverse roles in cell proliferation. This work mainly aimed to study the functions of HMGB2 on cervical cancer cells proliferation. HMGB2 was highly expressed in cervical cancer tissue. The results of real‐time polymerase chain reaction and Western blot analysis showed that HMGB2 was expressed in all the five cervical cancer cells (HeLa, CaSki, SiHa, C‐33A, and C4‐1 cells). In addition, HMGB2 overexpression obviously improved cell viability and promoted cell cycle progression, which suggested that HMGB2 could promote proliferation of cervical cancer cells. Moreover, HMGB2 overexpression increased the level of p‐AKT and reduced the levels of p21 and p27. However, HMGB2 downregulation had contrary influences on cell proliferation, cell cycle distribution and the levels of p‐AKT, p21, and p27. Notably, LY294002, as an inhibitor of AKT signaling pathway, could significantly weaken the effects of HMGB2 overexpression, which indicated that HMGB2 might promote cell proliferation by activating AKT signaling pathway. Therefore, HMGB2 was hopeful to be a candidate as a new biomarker and therapy target for cervical cancer.
Absent in melanoma 2 suppresses epithelial‐mesenchymal transition via Akt and inflammasome pathways in human colorectal cancer cells
Authors: Yang Yunjia , Zhang Minda , Jin Chenyu , Ding Yang , Yang Mengdi , Wang Rui , Zhou Yunjiang , Zhou Yang , Li Tao , Wang Keke , Hu Rong 
Published: June 2019

AbstractAbsent in melanoma 2 (AIM2) is a critical component in natural immunity system and is closely related to cancer initiation and development. It has been shown that AIM2 inhibited colorectal cancer (CRC) development and cell proliferation. It remains unresolved how AIM2 acts on CRC metastasis. In this study, we assessed migration, invasion ability, and epithelial‐mesenchymal transition (EMT) program upon AIM2 overexpression or knockdown in human CRC cells. Transwell assay demonstrated that upregulation of AIM2 reduced cell migration and invasion. Epithelial marker E‐cadherin was augmented and mesenchymal markers vimentin, as well as Snail, were examined decreased by Western blot, real‐time polymerase chain reaction, and immunofluorescence. Correspondingly, knockdown of AIM2 led to a reverse consequence. In addition, AIM2 regulated Akt phosphorylation and effects of AIM2 on cell invasion and EMT were recovered after administration of Akt inhibitor, suggesting that AIM2 suppressed EMT dependent on Akt pathway. In addition, caspase‐1 inhibitor exposure indicated that AIM2 abrogated EMT through the inflammasome pathway as well. In summary, AIM2 suppressed EMT via Akt and inflammasome pathways in human CRC cells.
Bin1 antibody lowers the expression of phosphorylated Tau in Alzheimer's disease
Authors: Thomas Sunil , Hoxha Kevther , Tran Allison , Prendergast George C. 
Published: June 2019

AbstractAlzheimer's disease (AD) is an irreversible, progressive brain disorder responsible for memory loss leading to the inability to carry out the simplest tasks. AD is one of the leading causes of death in the United States. As yet there are no effective medications to treat this debilitating disease. In recent years, a human gene called bridging integrator 1 (BIN1) has emerged as one of the most important genes in affecting the incidence of sporadic AD. Bin1 can directly bind to Tau and mediates late onset AD risk by modulating Tau pathology. Recently our group found Bin1 antibody could exert drug‐like properties in an animal model of ulcerative colitis. We hypothesized that the Bin1 monoclonal antibody (mAb) could be used in the treatment of AD by lowering the levels of Tau in cell culture and animal models. Cell culture studies confirmed that the Bin1 mAb (99D) could lower the levels of phosphorylated Tau (pTau). Multiple mechanisms aided by endosomal proteins and Fc gamma receptors are involved in the uptake of Bin1 mAb into cells. In Tau expressing cell culture, the Bin1 mAb induces the proteasome machinery leading to ubiquitination of molecules thereby preventing cell stress. In vivo studies demonstrated that treatment of P301S mice expressing Tau with the Bin1 mAb survived longer than the untreated mice. Our data confirm that Bin1 mAb lowers the levels of pTau and could be a drug candidate in the treatment of AD.
Insights into the molecular regulatory network of pathomechanisms in osteochondroma
Authors: Yang Congyi , Zhang Ruiqian , Lin Hui , Wang Hongmei 
Published: June 2019

AbstractOsteochondroma is a benign autosomal dominant hereditary disease characterized by abnormal proliferation of cartilage in the long bone. It is divided into solitary osteochondroma and hereditary multiple exostoses (HMEs). The exostosin‐1 (EXT‐1) and exostosin‐2 (EXT‐2) gene mutations are well‐defined molecular mechanisms in the pathogenesis of HME. EXT‐1 and EXT‐2 encode glycosyltransferases that are necessary for the synthesis of heparin sulfate. Accumulating evidence suggests that mutations in the EXT family induce changes in isolated hypogonadotropic hypogonadism‐parathyroid hormone‐related protein, bone morphogenetic protein, and fibroblast growth factor signaling pathways. Studies have also found that a large number of microRNAs (miRNAs) are abnormally expressed in osteochondroma tissues, and some of them also participate in several major signaling pathways. The regulation of miRNA expression could be another breakthrough in the treatment of osteochondroma. Although the pathogenesis of osteochondroma is very complicated, significant progress has been made in recent years. It is hoped that the pathogenesis of osteochondroma will be clearly understood and the most effective methods for the prevention and treatment of osteochondroma will be determined. This review provides an update on the recent progress in the interpretation of the underlying molecular mechanisms of osteochondroma.