bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of Optimal Calcium and Temperature Conditions for Quagga Mussel Filtration Rates as a Potential Predictor of Invasion
Authors: Gopalakrishnan Kishore K. , Kashian Donna R. 
Published: November 2019

Abstract
Quagga mussels (Dreissena rostriformis burgensis) are a highly invasive aquatic species to North America, capable of filtering large volumes of water and causing severe ecological and economic impacts. Their range has been expanding since they first invaded the Great Lakes in the 1980s. To predict their spread, it is crucial to understand environmental parameters, which facilitate their range expansion. Two factors likely to influence their distribution include calcium and temperature, because the former is vital for shell development and the latter for metabolic activity. When these factors are optimal for mussels' fitness, the filtration rate has the potential to be maximized if other environmental conditions are also favorable, thus enabling mussels to exploit their growth potential. Deviations from optimal conditions likely result in filtration-rate decline. We identify calcium concentrations and temperatures that maximize the mussel filtration rate for 2 phytoplankton species: Ankistrodesmus facaltus, a common food source for quagga mussels, and a less palatable Microcystis icthyoblabe. In laboratory experiments, filtration rates were measured through cell counts after 24 h of filtration when exposed to a range of temperatures between 2 and 30 °C, and calcium concentrations between 0 and 180 mg/L. Response surface methodology was used to identify a maximum filtration rate, which occurred at 22 mL/mg/h at 137 mg/L of calcium carbonate and 26 °C when fed Ankistrodesmus. To establish a quagga mussel population in a new water source, optimum conditions are required; thus, this information can be used to rank the relative susceptibility of water bodies to invasion by quagga mussels. Environ Toxicol Chem 2020;39:410–418. © 2019 SETAC
Abstract
Investigating the effect of the parameters of temperature and calcium concentration on the mussel filtration rate when fed with 2 different types of algae and determining the optimum parameters for the maximum filtration rate.
Pricing VIX derivatives with infinite‐activity jumps
Authors: Cao Jiling , Ruan Xinfeng , Su Shu , Zhang Wenjun 
Published: November 2019

AbstractIn this paper, we investigate a two‐factor VIX model with infinite‐activity jumps, which is a more realistic way to reduce errors in pricing VIX derivatives, compared with Mencía and Sentana (2013), J Financ Econ, 108, 367–391. Our two‐factor model features central tendency, stochastic volatility and infinite‐activity pure jump Lévy processes which include the variance gamma (VG) and the normal inverse Gaussian (NIG) processes as special cases. We find empirical evidence that the model with infinite‐activity jumps is superior to the models with finite‐activity jumps, particularly in pricing VIX options. As a result, infinite‐activity jumps should not be ignored in pricing VIX derivatives.
Patterns of protein expression in human head and neck cancer cell lines differ after proton vs photon radiotherapy
Authors: Wang Li , Yang Liuqing , Han Shichao , Zhu Jinming , Li Yuting , Wang Zeming , Fan You‐Hong , Lin Eric , Zhang Ruiping , Sahoo Narayan , Li Yupeng , Zhang Xiaodong , Wang Xiaochun , Li Tengfei , Zhu Xiaorong R. , Zhu Hongtu , Heymach John V. , Myers Jeffrey N. , Frank Steven J. 
Published: November 2019

AbstractBackgroundProton radiotherapy (PRT) may be a less toxic alternative to photon radiotherapy (XRT) for patients with head and neck squamous cell carcinoma (HNSCC). However, the molecular responses of HNSCC cells to PRT vs XRT are unclear.MethodsProteomics analyses of protein expression profiles by reverse‐phase protein arrays were done for two human papillomavirus [HPV]‐negative and two HPV+ cell lines. Expression patterns of 175 proteins involved in several signaling pathways were tested.ResultsCompared with PRT, XRT tended to induce lower expression of DNA damage repair—and cell cycle arrest‐related proteins and higher expression of cell survival‐ and proliferation‐related proteins.ConclusionsUnder these experimental conditions, PRT and XRT induced different protein expression and activation profiles. Further preclinical verification is needed, as are studies of tumor pathway mutations as biomarkers for choice of treatment or as radiosensitization targets to improve the response of HNSCC to PRT or XRT.
Japan's health care system faces a perfect storm
Authors: Kido Kaori , Tsukamoto Katsura 
Published: November 2019

SummaryAlthough Japan has implemented a universal health care system that is universal in terms of free access to health care services, it is managed by fragmented and financially insecure insurance societies that have cumulative deficits even with government subsidies. In terms of insurance premiums, the system is regressive to low‐income and unstable workers, and the social benefit scheme only captures 1.6% of this population. The Japanese government is continuously instituting new health care policies to reduce growing health care expenditures. Recent health care reforms may improve economic efficiency, but the changes remain limited to controlling access to health services and pricing measures.
The impact of climate change on U. K. river flows: A preliminary comparison of two generations of probabilistic climate projections
Authors: Kay Alison Lindsey , Watts Glenn , Wells Steven C. , Allen Stuart 
Published: November 2019

AbstractThe impacts of climate change on future river flows are a growing concern. Typically, impacts are simulated by driving hydrological models with climate model ensemble data. The U.K. Climate Projections 2009 (UKCP09) provided probabilistic projections, enabling a risk‐based approach to decision‐making under climate change. Recently, an update was released—UKCP18—so there is a need for information on how impacts may differ. The probabilistic projections from UKCP18 and UKCP09 are here applied using the change factor method with catchment‐based hydrological modelling for 10 catchments across England. Projections of changes in median, mean, high, and low flows are made for the 2050s, using the A1B emissions scenario from UKCP09 and UKCP18 as well as the RCP4.5 and RCP8.5 emissions scenarios from UCKP18. The results show that, in all catchments for all flow measures, the central estimate of change under UKCP18 is similar to that from UKCP09 (A1B emissions). However, the probabilistic uncertainty ranges from UKCP18 are, in all cases, greater than from UKCP09, despite UKCP18 having a smaller ensemble size than UKCP09. Although there are differences between the central estimates of change using UKCP18 RCP4.5, RCP8.5 and A1B emissions, there is considerable overlap in the uncertainty ranges. The results suggest that existing assessments of hydrological impacts remain relevant, though it will be necessary to evaluate sensitive decisions using the latest projections. The analysis will aid development of advice to users of current guidance based on UKCP09 and help make decisions about the prioritization of further hydrological impacts work using UKCP18, which should also apply other products from UKCP18 like the 12‐km regional data.
Insulin resistance is improved in high‐fat fed mice by photobiomodulation therapy at 630 nm
Authors: Silva Gabriela , Ferraresi Cleber , de Almeida Rodrigo T. , Motta Mariana L. , Paixão Thiago , Ottone Vinicius O. , Fonseca Ivana A. , Oliveira Murilo X. , Rocha‐Vieira Etel , Dias‐Peixoto Marco F. , Esteves Elizabethe A. , Coimbra Cândido C. , Amorim Fabiano T. , Magalhães Flávio de Castro 
Published: November 2019

AbstractPhotobiomodulation therapy (PBMT) in the infrared spectrum exerts positive effects on glucose metabolism, but the use of PBMT at the red spectrum has not been assessed. Male Swiss albino mice were divided into low‐fat control and high‐fat diet (HFD) for 12 weeks and were treated with red (630 nm) PBMT or no treatment (Sham) during weeks 9 to 12. PBMT was delivered at 31.19 J/cm2, 60 J total dose per day for 20 days. In HFD‐fed mice, PBMT improved glucose tolerance, insulin resistance and fasting hyperinsulinemia. PBMT also reduced adiposity and inflammatory infiltrate in adipose tissue. Phosphorylation of Akt in epididymal adipose tissue and rectus femoralis muscle was improved by PBMT. In epididymal fat PBMT reversed the reduced phosphorylation of AS160 and the reduced Glut4 content. In addition, PBMT reversed the alterations caused by HFD in rectus femoralis muscle on proteins involved in mitochondrial dynamics and β‐oxidation. In conclusion, PBMT at red spectrum improved insulin resistance and glucose metabolism in HFD‐fed mice.
Functional comparison of beating cardiomyocytes differentiated from umbilical cord‐derived mesenchymal/stromal stem cells and human foreskin‐derived induced pluripotent stem cells
Authors: Pushp Pallavi , Sahoo Bijayalaxmi , Ferreira Frederico C. , Sampaio Cabral Joaquim M. , Fernandes‐Platzgummer Ana , Gupta Mukesh K. 
Published: November 2019

AbstractIn recent years, stem cell‐based therapies shown to have promising effects on the clinical management of ischemic heart disease. Moreover, stem cells differentiation into cardiomyocytes (CMs) can overcome the cell source limitations. The current research involves the isolation and expansion of mesenchymal stem cells (MSCs) and induced pluripotent stem cells (iPSCs), their differentiation into CMs and subsequent construction of tissue‐engineered myocardium supported by random and aligned polycaprolactone (PCL) nanofibrous matrices (av. dia: 350–850 nm). Umbilical cord matrix (UCM)‐derived MSCs were isolated successfully by routine enzymatic digestion and a nonenzymatic explant culture method and characterized by their morphology, differentiation into different lineages, and surface marker expression. Treatment of UCM‐derived MSCs with 5‐azacytidine (5 μM) induced their differentiation into putative cardiac cells, as revealed by the expression of cardiac‐specific troponin T (cTnT), smooth muscles actin, myogenin (MYOG), smoothelin, cardiac α‐actin genes and cTnT, α‐actinin proteins by RT‐PCR and immunocytochemistry, respectively. However, no beating cells were observed in differentiated MSCs. On the other hand, adult human foreskin‐derived iPSCs cultured on Matrigel™—coated aligned PCL nanofibrous matrices showed anisotropic behavior along the PCL nanofibers and, upon differentiation, expressed cardiac‐specific cTnT (23.34 vs. 32.55%) proteins and showed more synchronized beating than those differentiated on Matrigel™—coated tissue culture coated polystyrene surfaces. Moreover, aligned PCL nanofibers are able to promote cells orientation parallel to the fibers, thus providing an effective way to control anisotropic nature under in vitro condition.
Peroxisome proliferator activated receptor γ promotes mineralization and differentiation in cementoblasts via inhibiting Wnt/β‐catenin signaling pathway
Authors: Hu Yingying , Wang Changning , Ha Shanshan , Zhu Ningjing , Cao Zhengguo , Song Yaling 
Published: November 2019

AbstractPeroxisome proliferator activated receptor γ (PPARγ) is a member of the nuclear receptor family of transcription factors, which involved in inflammation regulating and bone remodeling. Rare studies explored the effects of PPARγ on mineralization and differentiation in cementoblasts. To explore the potential approaches to repair the damaged periodontal tissues especially for cementum, the present study aims to investigate the effects and the regulating mechanism of PPARγ on mineralization and differentiation in cementoblasts. Murine cementoblast cell lines (OCCM‐30) were cultured in basic medium for 24 hours/48 hours or in mineralization medium for 3/7/10 days, respectively at addition of dimethyl sulphoxide, rosiglitazone (PPARγ agonist), GW9662 (PPARγ antagonist), lithium chloride (LiCl), tumor necrosis factor‐α (TNF‐α), or respective combination. Expression of mineralization genes alkaline phosphatase (ALP), runt related transcription factors 2 (RUNX2), and osteocalcin (OCN) were detected by quantitative real‐time polymerase chain reaction or/and Western blot. ALP staining and alizarin red staining were used to evaluate the mineralization in OCCM‐30 cells. The change of β‐catenin expression and translocation in cytoplasm/nucleus was analyzed by Western blot and immunofluorescence. The results showed that PPARγ agonist rosiglitazone improved the expression of ALP, RUNX2, and OCN, deepened ALP staining, increased mineralized nodules formation, and decreased β‐catenin expression in the nucleus. LiCl, an activator of the Wnt signaling pathway, inhibited the expression of mineralization genes and reversed the upregulated expression of mineralization genes resulted from rosiglitazone. Under inflammatory microenvironment, rosiglitazone not only suppressed the expression of interleukin‐1β caused by TNF‐α, but improved the expression of mineralization genes in OCCM‐30 cells. In conclusion, PPARγ could promote mineralization and differentiation in cementoblasts via inhibiting the Wnt/β‐catenin signaling pathway, which would shed new light on the treatment of periodontitis and periodontal tissue regeneration.
miR‐760 exerts an antioncogenic effect in esophageal squamous cell carcinoma by negatively driving fat metabolism via targeting c‐Myc
Authors: Yang Xuetao , Zhang Cheng , Tie Hongtao , Luo Jun , Wang Yiyang , Wu Qingchen 
Published: November 2019

AbstractmiR‐760 is downregulated in various human tumors, and fat metabolism disorder correlates with tumor progression, especially anomalism of key fat metabolic enzymes that are positively modulated by c‐Myc. The aim of our study is to elucidate the presumptive molecular mechanisms of miR‐760‐mediated esophageal squamous cell carcinoma (ESCC) cell function and to assess the therapeutic significance of miR‐760 in ESCC patients. Quantitative real‐time PCR (RT‐qPCR) analysis indicated that miR‐760 was significantly downexpressed in ESCC tissues and cell lines. Cell counting kit‐8 (CCK‐8) assay, colony formation assay, transwell assay, and flow cytometry denoted that induced ectopic overexpression of miR‐760 dramatically inhibited ESCC cells proliferation, attenuated migration, and invasion facilitated apoptosis in vitro. Mechanistically, c‐Myc predicted using bioinformatics was identified as a potential target gene of miR‐760 by luciferase reporter assay. Furthermore, mRNA and protein expression levels of c‐Myc and key fat metabolic enzymes were downregulated with miR‐760 mimics. The above investigation results, responsible for the antineoplastic properties of miR‐760 in ESCC, preliminarily highlighted that the hypothetical signal amongst miR‐760, c‐Myc, and key fat metabolic enzymes may develop a novel diagnostic marker, therapeutic target, and independent prognostic indicator.
An overview about DNA methylation in childhood obesity: Characteristics of the studies and main findings
Authors: Lima Rafael Silva , de Assis Silva Gomes Juliana , Moreira Paula Rocha 
Published: November 2019

AbstractChildhood obesity is a global burden affecting millions of children worldwide. It is well‐known that the adiposity profile in children is critical for future occurrence of diseases. As a multifactorial disease, obesity is associated with genetic and environmental factors. Epigenetic mechanisms link the plethora of environmental clues to a given phenotype. DNA methylation is the most studied epigenetic mark and its importance in several diseases was acknowledged. In childhood obesity, specifically, the studies show a consistent association between adiposity and methylation at the gene and genome‐wide scales. The relationship between DNA methylation and childhood obesity has been proved strong for some genes and pathways. However, the studies are heterogeneous in their design, methodologies, and results. The aim of this review is to discuss this heterogeneity and point out some aspects that should be considered in future studies to clarify the role of DNA methylation in childhood obesity.
miR‐146b Reverses epithelial‐mesenchymal transition via targeting PTP1B in cisplatin‐resistance human lung adenocarcinoma cells
Authors: Han Qian , Cheng Peng , Yang Hongjie , Liang Hengpo , Lin Fengchun 
Published: November 2019

AbstractEpithelial‐mesenchymal transformation (EMT) is associated with drug resistance in human lung adenocarcinoma cells, but its specific mechanism has not been clarified. In this study, we investigated the effect of miRNA‐146b on EMT in cisplatin (DDP) resistant human lung adenocarcinoma cells and the corresponding mechanism. Cisplatin resistant (CR) human lung adenocarcinoma cells (A549/DDP and H1299/DDP) were established, and the EMT characteristics and invasion and metastasis ability of CR cells were determined by tumor cell‐related biological behavior experiments. The role of miR‐146b in EMT of CR cells was determined by in vitro functional test. The targeted binding of miR‐146b to protein tyrosine phosphatase 1B (PTP1B) was verified by biological information and double luciferin gene reporting experiments. The effect of miR‐146b on tumor growth and EMT phenotype in vivo was investigated by establishing the xenotransplantation mouse model. Compared with the control group, H1299/DDP and A549/DDP cells showed the enhanced EMT phenotypes, invasion and migration ability. Besides, miR‐146b was lowly expressed in H1299/DDP and A549/DDP cells. More importantly, overexpressed miR‐146b could specifically bind to PTP1B, thus inhibiting the EMT process and ultimately reducing CR in H1299/DDP and A549/DDP cells. Finally, overexpressed miR‐146b observably inhibited tumor growth in xenograft model mice and inhibited the EMT phenotype of A549/DDP cells in vivo by regulating the expressions of EMT‐related proteins. Overexpressed miR‐146b could reverse the EMT phenotype of CR lung adenocarcinoma cells by targeting PTP1B, providing new therapeutic directions for CR of lung adenocarcinoma cells.
Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway
Authors: Luo Man , Yan Dongsheng , Sun Qingsong , Tao Jiali , Xu Liang , Sun Hong , Zhao Hongmei 
Published: November 2019

AbstractSepsis‐induced myocardial dysfunction (SIMD) causes high mortality in seriously ill patients. Ginsenoside Rg1 has been proven to have effective anti‐inflammatory and antiapoptotic properties. However, the specific role of Rg1 in SIMD and the molecular mechanism remain unclear. Hence, we aimed to investigate the latent effects of ginsenoside Rg1 against SIMD and explore its underlying mechanisms. Male C57BL/6J mice and neonatal rat cardiomyocytes (NRCMs) were used as in vivo and in vitro models, respectively. Western blot analysis was used to detect the level of protein expression, and reverse transcription polymerase chain reaction was conducted to determine the messenger RNA expression of inflammatory factors. The terminal deoxynucleotidyl transferase‐mediated nick end labeling assay and flow cytometry were used to determine the apoptosis rate. Echocardiography was performed to assess cardiac function. The results showed that Rg1 improved cardiac function and attenuated lipopolysaccharide (LPS)‐induced apoptosis and inflammation in mice. In addition, in NRCMs, Rg1 downregulated the expression of LPS‐induced inflammatory cytokines and reversed the increased expression of Toll‐like receptor 4 (TLR4), nuclear factor‐κB (NF‐κB), and NOD‐like receptor 3 (NLRP3). In addition, treatment with TLR4 small interfering RNA (siRNA), a p‐NF‐κB inhibitor, or NLRP3 siRNA suppressed LPS‐induced apoptosis and inflammation. In conclusion, Rg1 can attenuate LPS‐induced inflammation and apoptosis both in NRCMs and septic mice and restore impaired cardiac function. Moreover, Rg1 may exert its effect via blocking the TLR4/NF‐κB/NLRP3 pathway.
Study on amniotic fluid metabolism in the second trimester of Trisomy 21
Authors: Liu Xiaoting , Quan Sheng , Fu Yurong , Wang Weiwei , Zhang Wenling , Wang Xiaofei , Zhang Chenxi , Xiang Daijun , Zhang Liwen , Wang Chengbin 
Published: November 2019

AbstractBackgroundTrisomy 21 is a common aneuploid condition in humans and accounts for approximately one quarter of all aneuploid live births. To date, early diagnosis of Trisomy 21 remains a challenging task. Metabolomics may prove an innovative tool to study the early pathophysiology of Trisomy 21 at a functional level.MethodsUltra‐performance liquid chromatography coupled with mass spectrometer (UPLC‐MS) was used for untargeted metabolomic analysis of amniotic fluid samples from women having normal and trisomy 21 fetuses.ResultsMany significantly changed metabolites were identified between amniotic fluid samples from Trisomy 21 pregnancies and normal euploid pregnancies, such as generally lower levels of several steroid hormones and their derivatives, higher levels of glutathione catabolites coupled with lower levels of gamma‐glutamyl amino acids, and increased levels of phospholipid catabolites, sugars, and dicarboxylic acids. The identification of a human milk oligosaccharide in amniotic fluid may worth further investigation, since confirmation of this observation may have significant implications for regulation of fetal development.ConclusionsThe metabolisms in amniotic fluid from Trisomy 21 and normal pregnancies are quite different, and some of the significantly changed metabolites may be considered as candidates of early diagnostic biomarkers for Trisomy 21.
Inhibition of microRNA‐150‐5p alleviates cardiac inflammation and fibrosis via targeting Smad7 in high glucose‐treated cardiac fibroblasts
Authors: Che Hui , Wang Yueqiu , Li Yang , Lv Jie , Li Hui , Liu Yining , Dong Ruixue , Sun Yongle , Xu Xiaodan , Zhao Jie , Wang Lihong 
Published: November 2019

AbstractHyperglycemia‐induced cardiac fibrosis is a prominent characteristic of diabetic cardiomyopathy. Changes in proinflammatory cytokines have been shown to lead to cardiac fibrosis in patients with diabetes mellitus. This study aimed to investigate the role of miR‐150‐5p in mediating cardiac inflammation and fibrosis in cardiac fibroblasts (CFs). Herein, we found that high‐glucose (HG) treatment significantly induced cardiac inflammation, as manifested by increased proinflammatory cytokine production (IL‐1β) and NF‐κB activity in CFs. Moreover, HG markedly aggravated cardiac fibrosis and increased levels of fibrotic markers (CTGF, FN, α‐SMA) and extracellular matrix proteins (Col‐I, Col‐III) in CFs. At the same time, HG disturbed the TGF‐β1/Smad signaling pathway, as evidenced by increases in TGF‐β1 and p‐Smad2/3 levels and decreases in Smad7 levels in CFs. Furthermore, we found that miR‐150‐5p was upregulated by HG, which negatively regulated Smad7 expression at the posttranscription level. Further study demonstrated that cardiac inflammation and fibrosis in CFs were corrected following miR‐150‐5p knockdown, but exacerbated by miR‐150‐5p overexpression. These data indicated that miR‐150‐5p inhibition could ameliorate NF‐κB‐related inflammation and TGF‐β1/Smad‐induced cardiac fibrosis through targeting Smad7. Thus, miR‐150‐5p may be a novel promising target for treating diabetic cardiomyopathy.