bluuebunny/crossref_metadata_2025_split huggingface dataset:
Data mining in the Dutch Oil and Gas Portal: a case study on the reservoir properties of the Volpriehausen Sandstone interval
Authors: van Kempen B. M. M. , Mijnlieff H. F. , van der Molen J. 
Published: March 2018

Abstract
This paper presents the results of a data mining exercise on core measurements and reports of the Triassic Lower Volpriehausen Sandstone Member (RBMVL) in The Netherlands. The availability of a large accurate online dataset via the Dutch Oil and Gas Portal (NLOG) enables the definition of general reservoir property trends on a regional–subregional scale. Accurately defined trends are capable of restricting the uncertainty range of key parameters in exploration studies (e.g. porosity and permeability), and thus of reducing risk. Plotting core porosity v. core permeability resulted in a curved data cloud on a log-normal plot. Although porosity–permeability relationships are often defined by straight lines, the dataset in this study shows that a curved relationship results in a better fit with permeability measurements over the entire porosity range. Two methods were applied to define a porosity–depth relationship for sandstones of the RBMVL. The results of both methods confirm, and enable quantification of, the well-known trend of decreasing porosity with depth. By assigning grain density attributes to the core measurements, the dependency of the porosity–depth relationship on sedimentary facies and diagenesis type/grade could be determined. This case study demonstrates the power of this free online dataset in understanding reservoir quality.
Oscillometry and pulmonary MRI measurements of ventilation heterogeneity in obstructive lung disease: relationship to quality of life and disease control
Authors: Young Heather M. , Guo Fumin , Eddy Rachel L. , Maksym Geoffrey , Parraga Grace 
Published: March 2018

Ventilation heterogeneity is a hallmark finding in obstructive lung disease and may be evaluated using a variety of methods, including multiple-breath gas washout and pulmonary imaging. Such methods provide an opportunity to better understand the relationships between structural and functional abnormalities in the lungs, and their relationships with important clinical outcomes. We measured ventilation heterogeneity and respiratory impedance in 100 subjects [50 patients with asthma, 22 ex-smokers, and 28 patients with chronic obstructive pulmonary disease (COPD)] using oscillometry and hyperpolarized 3He magnetic resonance imaging (MRI) and determined their relationships with quality of life scores and disease control/exacerbations. We also coregistered MRI ventilation maps to a computational airway tree model to generate patient-specific respiratory impedance predictions for comparison with experimental measurements. In COPD and asthma patients, respectively, forced oscillation technique (FOT)-derived peripheral resistance (5–19 Hz) and MRI ventilation defect percentage (VDP) were significantly related to quality of life (FOT: COPD ρ = 0.4, P = 0.004; asthma ρ = −0.3, P = 0.04; VDP: COPD ρ = 0.6, P = 0.003; asthma ρ = −0.3, P = 0.04). Patients with poorly controlled asthma (Asthmatic Control Questionnaire >2) had significantly increased resistance (5 Hz: P = 0.01; 5–19 Hz: P = 0.006) and reactance (5 Hz: P = 0.03). FOT-derived peripheral resistance (5–19 Hz) was significantly related to VDP in patients with asthma and COPD patients (asthma: ρ = 0.5, P < 0.001; COPD: ρ = 0.5, P = 0.01), whereas total respiratory impedance was related to VDP only in patients with asthma (resistance 5 Hz: ρ = 0.3, P = 0.02; reactance 5 Hz: ρ = −0.5, P < 0.001). Model-predicted and FOT-measured reactance (5 Hz) were correlated in patients with asthma (ρ = 0.5, P = 0.001), whereas in COPD patients, model-predicted and FOT-measured resistance (5–19 Hz) were correlated (ρ = 0.5, P = 0.004). In summary, in patients with asthma and COPD patients, we observed significant, independent relationships for FOT-measured impedance and MRI ventilation heterogeneity measurements with one another and with quality of life scores. NEW & NOTEWORTHY In 100 patients, including patients with asthma and ex-smokers, 3He MRI ventilation heterogeneity and respiratory system impedance were correlated and both were independently related to quality of life scores and asthma control. These findings demonstrated the critical relationships between respiratory system impedance and ventilation heterogeneity and their role in determining quality of life and disease control. These observations underscore the dominant role that abnormalities in the lung periphery play in ventilation heterogeneity that results in patients’ symptoms.
Effect of contractile activity on PGC-1α transcription in young and aged skeletal muscle
Authors: Carter Heather N. , Pauly Marion , Tryon Liam D. , Hood David A. 
Published: March 2018

Mitochondrial impairments are often noted in aged skeletal muscle. The transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is integral to maintaining mitochondria, and its expression declines in aged muscle. It remains unknown whether this is due to a transcriptional deficit during aging. Our study examined PGC-1α transcription in muscle from young and old F344BN rats. Using a rat PGC-1α promoter-reporter construct, we found that PGC-1α transcription was reduced by ∼65% in aged TA muscle, accompanied by decreases in PGC-1α mRNA and transcript stability. Altered expression patterns in PGC-1α transcription regulatory factors, including nuclear respiratory factor 2, upstream transcription factor 1, activating transcription factor 2, and yin yang 1, were noted in aged muscle. Acute contractile activity (CA) followed by recovery was employed to examine whether PGC-1α transcription could be activated in aged muscle similar to that observed in young muscle. AMPK and p38 signaling was attenuated in aged muscle. CA evoked an upregulation of PGC-1α transcription in both young and aged groups, whereas mRNAs encoding PGC-1α and cytochrome oxidase subunit IV were induced during the recovery period. Global DNA methylation, an inhibitory event for transcription, was enhanced in aged muscle, likely a result of elevated methyltransferase enzyme Dnmt3b in aged muscle. Successive bouts of CA for 7 days to evaluate longer-term consequences resulted in a rescue of PGC-1α and downstream mRNAs in aged muscle. Our data indicate that diminished mitochondria in aged muscle is due partly to a deficit in PGC-1α transcription, a result of attenuated upstream signaling. Contractile activity is an appropriate countermeasure to restore PGC-1α expression and mitochondrial content in aged muscle.NEW & NOTEWORTHY PGC-1α is a regulator of mitochondrial biogenesis in muscle. We demonstrate that PGC-1α expression is reduced in aging muscle due to decreases in transcriptional and posttranscriptional mechanisms. The transcriptional deficit is due to alterations in transcription factor expression, reduced signaling, and DNA methylation. Acute exercise can initiate signaling to reverse the transcriptional defect, restoring PGC-1α expression toward young values, suggesting a mechanism whereby aged muscle can respond to exercise for the promotion of mitochondrial biogenesis.
A miR-29b Byproduct Sequence Exhibits Potent Tumor-Suppressive Activities via Inhibition of NF-κB Signaling in KRAS-Mutant Colon Cancer Cells
Authors: Inoue Akira , Mizushima Tsunekazu , Wu Xin , Okuzaki Daisuke , Kambara Nanami , Ishikawa Sho , Wang Jiaqi , Qian Yamin , Hirose Haruka , Yokoyama Yuhki , Ikeshima Ryo , Hiraki Masayuki , Miyoshi Norikatsu , Takahashi Hidekazu , Haraguchi Naotsugu , Hata Taishi , Matsuda Chu , Doki Yuichiro , Mori Masaki , Yamamoto Hirofumi 
Published: March 2018

Abstract
We previously demonstrated that miR-29b-3p is a hopeful miRNA-based therapy against colorectal cancer. In this study, we aimed to clarify a value of miR-29b-1-5p as a next-generation treatment, especially for KRAS-mutant colorectal cancer. RT-PCR assay showed that the expression of miR-29b-3p was high, and its partner strand, miR-29b-1-5p, level was only negligible in clinical colorectal cancer samples. Mimic-miR-29b-1-5p significantly inhibited proliferation of KRAS-mutant colorectal cancer cell lines DLD1 and SW480 and KRAS wild-type HT29 cells. Proliferative activity was further examined by either miR-29b-1-5p strand or its opposite complementary sequence because miR-29b-1-5p is a passenger miRNA and may have no physiologic function. We found that completely opposite complementary strand to miR-29b-1-5p, but not miR-29b-1-5p, possessed a potent antitumor effect and named this byproduct miRNA sequence “MIRTX.” MIRTX directly targeted the 3′-UTR of CXCR2 and PIK3R1 mRNA and suppressed the NF-κB signaling pathway in KRAS-mutated colorectal cancer cells. MIRTX induced apoptosis in DLD1 with downregulation of antiapoptotic BCL2, BCL-xL, and MCL1 and upregulation of cleaved caspase-3 and cleaved PARP. In mouse xenograft models, systemic administration of MIRTX using a super carbonate apatite as a delivery vehicle significantly inhibited tumor growth of DLD1 and HT29 cells without any particular toxicities. In conclusion, these findings indicate that inhibition of NF-κB signaling by this novel miRNA-based therapeutic could be a promising treatment against refractory KRAS-mutant colorectal cancer and KRAS wild-type colorectal cancer. Mol Cancer Ther; 17(5); 977–87. ©2018 AACR.
D-2-Hydroxyglutarate Is Necessary and Sufficient for Isocitrate Dehydrogenase 1 Mutant–Induced MIR148A Promoter Methylation
Authors: Li Tie , Cox Christopher D. , Ozer Byram H. , Nguyen Nhung T. , Nguyen HuyTram N. , Lai Thomas J. , Li Sichen , Liu Fei , Kornblum Harley I. , Liau Linda M. , Nghiemphu Phioanh L. , Cloughesy Timothy F. , Lai Albert 
Published: March 2018

Abstract
Mutant isocitrate dehydrogenase (IDH) 1/2 converts α-ketoglutarate (α-KG) to D-2 hydroxyglutarate (D-2-HG), a putative oncometabolite that can inhibit α-KG–dependent enzymes, including ten-eleven translocation methylcytosine dioxygenase (TET) DNA demethylases. We recently established that miRNAs are components of the IDH1 mutant–associated glioma CpG island methylator phenotype (G-CIMP) and specifically identified MIR148A as a tumor-suppressive miRNA within G-CIMP. However, the precise mechanism by which mutant IDH induces hypermethylation of MIR148A and other G-CIMP promoters remains to be elucidated. In this study, we demonstrate that treatment with exogenous D-2-HG induces MIR148A promoter methylation and transcriptional silencing in human embryonic kidney 293T (293T) cells and primary normal human astrocytes. Conversely, we show that the development of MIR148A promoter methylation in mutant IDH1–overexpressing 293T cells is abrogated via treatment with C227, an inhibitor of mutant IDH1 generation of D-2-HG. Using dot blot assays for global assessment of 5-hydroxymethylcytosine (5-hmC), we show that D-2-HG treatment reduces 5-hmC levels, whereas C227 treatment increases 5-hmC levels, strongly suggesting TET inhibition by D-2-HG. Moreover, we show that withdrawal of D-2-HG treatment reverses methylation with an associated increase in MIR148A transcript levels and transient generation of 5-hmC. We also demonstrate that RNA polymerase II binds endogenously to the predicted promoter region of MIR148A, validating the hypothesis that its transcription is driven by an independent promoter.
Implications: Establishment of D-2-HG as a necessary and sufficient intermediate by which mutant IDH1 induces CpG island methylation of MIR148A will help with understanding the efficacy of selective mutant IDH1 inhibitors in the clinic. Mol Cancer Res; 16(6); 947–60. ©2018 AACR.
USP28 Deficiency Promotes Breast and Liver Carcinogenesis as well as Tumor Angiogenesis in a HIF-independent Manner
Authors: Richter Kati , Paakkola Teija , Mennerich Daniela , Kubaichuk Kateryna , Konzack Anja , Ali-Kippari Heidi , Kozlova Nina , Koivunen Peppi , Haapasaari Kirsi-Maria , Jukkola-Vuorinen Arja , Teppo Hanna-Riikka , Dimova Elitsa Y. , Bloigu Risto , Szabo Zoltan , Kerkelä Risto , Kietzmann Thomas 
Published: March 2018

Abstract
Recent studies suggest that the ubiquitin-specific protease USP28 plays an important role in cellular repair and tissue remodeling, which implies that it has a direct role in carcinogenesis. The carcinogenic potential of USP28 was investigated in a comprehensive manner using patients, animal models, and cell culture. The findings demonstrate that overexpression of USP28 correlates with a better survival in patients with invasive ductal breast carcinoma. Mouse xenograft experiments with USP28-deficient breast cancer cells also support this view. Furthermore, lack of USP28 promotes a more malignant state of breast cancer cells, indicated by an epithelial-to-mesenchymal (EMT) transition, elevated proliferation, migration, and angiogenesis as well as a decreased adhesion. In addition to breast cancer, lack of USP28 in mice promoted an earlier onset and a more severe tumor formation in a chemical-induced liver cancer model. Mechanistically, the angio- and carcinogenic processes driven by the lack of USP28 appeared to be independent of HIF-1α, p53, and 53BP1.
Implications: The findings of this study are not limited to one particular type of cancer but are rather applicable for carcinogenesis in a more general manner. The obtained data support the view that USP28 is involved in tumor suppression and has the potential to be a prognostic marker. Mol Cancer Res; 16(6); 1000–12. ©2018 AACR.
Olaparib-induced Adaptive Response Is Disrupted by FOXM1 Targeting that Enhances Sensitivity to PARP Inhibition
Authors: Fang Pingping , Madden Jill A. , Neums Lisa , Moulder Ryan K. , Forrest M. Laird , Chien Jeremy 
Published: March 2018

Abstract
FOXM1 transcription factor network is activated in over 84% of cases in high-grade serous ovarian cancer (HGSOC), and FOXM1 upregulates the expression of genes involved in the homologous recombination (HR) DNA damage and repair (DDR) pathway. However, the role of FOXM1 in PARP inhibitor response has not yet been studied. This study demonstrates that PARP inhibitor (PARPi), olaparib, induces the expression and nuclear localization of FOXM1. On the basis of ChIP-qPCR, olaparib enhances the binding of FOXM1 to genes involved in HR repair. FOXM1 knockdown by RNAi or inhibition by thiostrepton decreases FOXM1 expression, decreases the expression of HR repair genes, such as BRCA1 and RAD51, and enhances sensitivity to olaparib. Comet and PARP trapping assays revealed increases in DNA damage and PARP trapping in FOXM1-inhibited cells treated with olaparib. Finally, thiostrepton decreases the expression of BRCA1 in rucaparib-resistant cells and enhances sensitivity to rucaparib. Collectively, these results identify that FOXM1 plays an important role in the adaptive response induced by olaparib and FOXM1 inhibition by thiostrepton induces “BRCAness” and enhances sensitivity to PARP inhibitors.
Implications: FOXM1 inhibition represents an effective strategy to overcome resistance to PARPi, and targeting FOXM1-mediated adaptive pathways may produce better therapeutic effects for PARP inhibitors. Mol Cancer Res; 16(6); 961–73. ©2018 AACR.
Cholesterol Esterification Inhibition Suppresses Prostate Cancer Metastasis by Impairing the Wnt/β-catenin Pathway
Authors: Lee Hyeon Jeong , Li Jie , Vickman Renee E. , Li Junjie , Liu Rui , Durkes Abigail C. , Elzey Bennett D. , Yue Shuhua , Liu Xiaoqi , Ratliff Timothy L. , Cheng Ji-Xin 
Published: March 2018

Abstract
Dysregulation of cholesterol is a common characteristic of human cancers including prostate cancer. This study observed an aberrant accumulation of cholesteryl ester in metastatic lesions using Raman spectroscopic analysis of lipid droplets in human prostate cancer patient tissues. Inhibition of cholesterol esterification in prostate cancer cells significantly suppresses the development and growth of metastatic cancer lesions in both orthotopic and intracardiac injection mouse models. Gene expression profiling reveals that cholesteryl ester depletion suppresses the metastatic potential through upregulation of multiple regulators that negatively impact metastasis. In addition, Wnt/β-catenin, a vital pathway for metastasis, is downregulated upon cholesteryl ester depletion. Mechanistically, inhibition of cholesterol esterification significantly blocks secretion of Wnt3a through reduction of monounsaturated fatty acid levels, which limits Wnt3a acylation. These results collectively validate cholesterol esterification as a novel metabolic target for treating metastatic prostate cancer. Mol Cancer Res; 16(6); 974–85. ©2018 AACR.
Description of the first juvenile stage of the fiddler crab Minuca mordax (Smith, 1870) (Crustacea, Decapoda, Ocypodidae)
Authors: Martins Salise Brandt , Marochi Murilo Zanetti , Masunari Setuko 
Published: March 2018

The first stage of the fiddler crab Minuca mordax is described here. Zoea larvae obtained from four ovigerous female were reared in the laboratory until the development of the first crab stage. The development from zoea I to the first juvenile instar lasted 35 days after hatching. The first crab stage of Minuca mordax can be morphologically distinguished from those of Minuca burgersi and Leptuca cumulanta by a 2‑segmented antennule endopod (3‑segmented in M. burgersi, unsegmented in L. cumulanta), an unsegmented maxillule endopod (2‑segmented in M. burgersi and L. cumulanta), and a 4‑segmented first and second maxilliped endopod (respectively unsegmented and 5‑segmented in M. burgersi and L. cumulanta). The three species have the following characters in common: segmented peduncle of antennule 2; endopod of antennule unsegmented; presence of aesthetascs on the antennule; peduncle of antenna 3‑segmented; flagellum of antenna 6‑segmented; mandible 3‑segmented; maxilla with coxal and basal endite bilobed; first, second and third maxillae with exopod 2‑segmented and abdomen with six somites that are wider than long.
Idades U-Pb de zircão detríticos e suas implicações na proveniência de sedimentos da Formação Penedo, Bacia de Sergipe-Alagoas, NE Brasil
Authors: Melo Alice Maria Queiroz de , Rosa Maria De Lourdes da Silva , Conceição Herbet 
Published: March 2018

A Formação Penedo representa um sistema fluviodeltaico de padrão entrelaçado pertencente ao estágio rifte da Bacia de Sergipe-Alagoas (BSA). Este trabalho foi realizado na seção aflorante, que deu o nome a esta unidade, localizada na cidade de Penedo, Estado de Alagoas, e denominada PDO-01. A metodologia de estudo envolveu análise de paleocorrente aliada à datação U-Pb de cristais de zircão detríticos por Espectrometria de Massa por Ablação a Laser (LA-ICP-MS). O registro sedimentar de paleocorrentes indicou aporte vindo de norte, enquanto os cristais analisados apresentaram idades variando do Mesoarqueano (3098 ± 33 Ma) ao Paleozoico (530 ± 12 Ma), que foram reunidas em cinco grupos (G1 a G5). Dessa análise conjunta foram propostas as seguintes fontes de proveniência: para o primeiro grupo (G1), os granitos neoproterozoicos (~670 Ma) pertencentes ao Domínio Pernambuco-Alagoas; para o segundo grupo (G2), as rochas do Complexo Cabrobó (~0,9 – 1,2 Ga); para o terceiro grupo (G3), as rochas do Complexo Arapiraca com idades paleoproterozoicas (~1,6 – 2,2 Ga); e para o quarto e o quinto grupos (G4 e G5), as rochas do Complexo Nicolau Campo Grande com idades neoarqueanas (~2,4 – 3,0 Ga).
Senescence Alters PPARγ (Peroxisome Proliferator–Activated Receptor Gamma)-Dependent Fatty Acid Handling in Human Adipose Tissue Microvascular Endothelial Cells and Favors Inflammation
Authors: Briot Anaïs , Decaunes Pauline , Volat Fanny , Belles Chloé , Coupaye Muriel , Ledoux Séverine , Bouloumié Anne 
Published: March 2018

Objective—
Adipose tissue (AT) dysfunction associated with obesity or aging is a major cause for lipid redistribution and the progression of cardiometabolic disorders. Our goal is to decipher the contribution of human AT microvascular endothelial cells (ECs) in the maintenance of fatty acid (FA) fluxes and the impact of senescence on their function.

Approach and Results—
We used freshly isolated primary microvascular ECs from human AT. Our data identified the endothelial FA handling machinery including FATPs (FA transport proteins) FATP1, FATP3, FATP4, and CD36 as well as FABP4 (FA binding protein 4). We showed that PPARγ (peroxisome proliferator–activated receptor gamma) regulates the expression of FATP1, CD36, and FABP4 and is a major regulator of FA uptake in human AT EC (hATEC). We provided evidence that endothelial PPARγ activity is modulated by senescence. Indeed, the positive regulation of FA transport by PPARγ agonist was abolished, whereas the emergence of an inflammatory response was favored in senescent hATEC. This was associated with the retention of nuclear FOXO1 (forkhead box protein O1), whereas nuclear PPARγ translocation was impaired.

Conclusions—
These data support the notion that PPARγ is a key regulator of primary hATEC function including FA handling and inflammatory response. However, the outcome of PPARγ activation is modulated by senescence, a phenomenon that may impact the ability of hATEC to properly respond to and handle lipid fluxes. Finally, our work highlights the role of hATEC in the regulation of FA fluxes and reveals that dysfunction of these cells with accelerated aging is likely to participate to AT dysfunction and the redistribution of lipids.
Trajectories of Health-Related Quality of Life in Coronary Artery Disease
Authors: Sajobi Tolulope T. , Wang Meng , Awosoga Oluwagbohunmi , Santana Maria , Southern Danielle , Liang Zhiying , Galbraith Diane , Wilton Stephen B. , Quan Hude , Graham Michelle M. , James Matthew T. , Ghali William A. , Knudtson Merrill L. , Norris Colleen 
Published: March 2018

Background:
Health-related quality of life (HRQOL) assessment is an important health outcome for measuring the efficacy of treatments and interventions for coronary artery disease (CAD). HRQOL is known to improve over the first year after interventions for CAD, but there is limited knowledge of the changes in HRQOL beyond 1 year. We investigated heterogeneity in long-term trajectories of HRQOL in patients with CAD.

Methods and Results:
Data were obtained from 6226 patients identified from the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease with at least 1-vessel CAD who underwent their first catheterization between 2006 and 2009. HRQOL was assessed using the Seattle Angina Questionnaire, a 19-item disease-specific measure of HRQOL for patients with CAD. Group-based trajectory analysis was used to identify various subgroups of Seattle Angina Questionnaire trajectories over time while adjusting for missing data through a longitudinal multiple imputation model. Multinomial logistic regression was used to identify the predictors of differences among the identified subgroups. Our analysis revealed significant improvements in HRQOL across all the 5 domains of Seattle Angina Questionnaire overtime for the whole data. Multitrajectory analyses revealed 4 HRQOL trajectory subgroups including high (25.1%), largely increased (32.3%), largely decreased (25.0%), and low (17.6%) trajectories. Age, sex, body mass index, diabetes mellitus, previous history of myocardial infarction, smoking, depression, anxiety, type of treatment received, and perceived social support were significant predictors of differences among these trajectory subgroups.

Conclusions:
This study highlights variations in longitudinal trajectories of HRQOL in patients with CAD. Despite overall improvements in HRQOL, about a quarter of our cohort experienced a significant decline in their HRQOL over the 5-year period. Understanding these HRQOL trajectories may help personalize prognostic information, identify patients and HRQOL domains on which clinical interventions are most beneficial, and support treatment decisions for patients with CAD.