bluuebunny/crossref_metadata_2025_split huggingface dataset:
Secondary Flows in the Return System of a Centrifugal Compressor Stage
Authors: Rossbach T. , Bisping J. , Grates D. R. , Jeschke P. , Hildebrandt A. , Franz H. 
Published: March 2020

Abstract
This paper presents an analysis of the flow in the return system of a centrifugal compressor with a flow coefficient of 0.15. Based on the detailed experimental and numerical data, the areas of high losses and potentials for improving the return system geometry are revealed. Special emphasis is placed on the interaction of the flow in the return system components, including the U-bend, the vaned return channel, and the final L-bend. Strong flow redistribution occurs due to the sharp curvature of the U-bend, forming a blockage area at the hub near the vane leading edge. This causes a strong passage vortex, which is further intensified by the pressure gradient induced by the L-bend. Additionally, the flow near the shroud accelerates due to the large blockage area near the hub at the exit of the U-bend, resulting in high friction losses. To identify the main causes of loss, a method was evolved. It was validated and supplied by pneumatic measurement data. On this basis, analytical approaches were taken to quantify the total pressure losses due to friction, secondary flows, incidence, and trailing edge flow. As a result, approximately 60% of the return system losses arise due to friction. Another 30–40% are caused by secondary flows. It can be concluded that the results of the investigation contribute to the understanding of the secondary flow structures inside a centrifugal compressor return system of high mass flowrates. By combining the knowledge acquired in respect to the sources of highest losses with the experimental data, a well-founded basis for future optimization is achieved and the validation of numerical approaches is possible.
Experimental Evaluation of Geopolymer, Nano-Modified, and Neat Class H Cement by Using Diametrically Compressive Tests
Authors: Kimanzi Raymos , Wu Yuxing , Salehi Saeed , Mokhtari Mehdi , Khalifeh Mahmoud 
Published: March 2020

AbstractCement is the prime barrier material to maintain zonal isolation during wellbore life-cycle. Different types of the cement have different performances on sealability. The primary objective of this study is evaluation of three types of cement systems, neat Class H, nano-synthetic graphite, and rock-based geopolymer cements, on interfacial bond integrity. Diametrical compressive tests are used on casing–cement–formation systems. Cement performances are tested in a conventional configuration (Berea Sandstone). A universal testing system is utilized to analyze the relationship applied load–axial strain and the digital image correlation (DIC) technique is used to generate the strain field maps. Based on the relationship and DIC results, bond strengths in different cement systems are evaluated. Additionally, microscope images provide insight explanations of the bond from micro-view. Based on the experimental results, failures of all cases initiate and propagate from the casing–cement interface. Then, radial cracks develop through the formation. This is because the mechanical interlocking bonds are formed only at the cement–sandstone interface to enhance the bond strength. The comparison of geopolymer and nano-modified cements with the conventional cement (neat Class H) shows that the unconventional cements have a lower maximum load and higher axial strain before failure of the samples. It indicates that both the two kinds of cements are more ductile than conventional cement and can support more deformation before the initiation of cracks.
Silica diagenesis promotes early primary hydrocarbon migration
Authors: Abu-Mahfouz Israa S. , Cartwright Joe , Idiz Erdem , Hooker John N. , Robinson Stuart A. 
Published: March 2020

AbstractWe present evidence that hydrocarbon source rocks can be preconditioned for primary hydrocarbon migration at an early stage of catagenesis by pore-scale processes linked to silica diagenesis. The evidence comes from a detailed petrographic and geochemical study of the Jordan Oil Shale (JOS), an immature to early mature, Upper Cretaceous to Paleogene source rock developed on the platform regions of central and southern Jordan. Diagenesis of biogenic silica led to silicification of the source rock interval and the growth of chert nodules. Localization of bitumen veins in reaction rims around these nodules is interpreted to indicate that silica diagenesis promotes the early mobilization of hydrocarbons from the geochemically identical, disseminated bitumen within the host mudstones. We propose a model in which early-formed bitumen migrated into neoforming mode I fractures that formed as a result of the crystallization pressure imposed from the growing chert nodule. Hydraulic fracturing occurred under elevated bitumen fluid pressures that approached lithostatic stress values under burial depths of the order of 1000 m. The recognition that silica diagenesis can promote the early migration of neoforming bitumen raises the possibility that primary hydrocarbon migration may occur earlier and at shallower depths than predicted by kinetic modeling approaches wherever silica diagenetic reactions are coeval with catagenesis.
Quantifying the volume increase and chemical exchange during serpentinization
Authors: Klein Frieder , Le Roux Véronique 
Published: March 2020

AbstractQuantifying the concurrent changes in rock volume and fluid composition during serpentinization remains a major challenge in assessing its physicochemical effects during continental rifting, seafloor spreading, and subduction. Here we conducted a series of 11 hydrothermal laboratory experiments where cylindrical cores of natural dunite, harzburgite, and pyroxenite were reacted with an aqueous solution at 300 °C and 35 MPa for up to 18 months. Using three-dimensional microcomputed tomography and thermogravimetry, we show that rock volume systematically increased with time and extent of reaction, leading to a volume increase of 44% (±8%) in altered rock domains after 10–18 months of serpentinization. The volume expansion was accompanied by Mg-Ca exchange between fluid and rock, while Fe and Si were largely conserved. We find that the protolith composition (olivine/orthopyroxene ratio) plays a significant role in controlling the fluid chemistry and the proportions of hydrous secondary minerals during serpentinization. Agreement between alteration mineralogy, composition of reacting fluids, and measured volume changes suggests that serpentinization under static conditions is a volume-increasing process in spite of demonstrable mass transfer. Volume expansion implies an increased water carrying capacity and buoyancy force of serpentinite per unit mass of protolith, while Mg-Ca exchange during serpentinization may affect the Mg/Ca ratio of seawater on Earth and possibly other ocean worlds.
Cerebral aneurysm treatment trends in National Inpatient Sample 2007–2016: endovascular therapies favored over surgery
Authors: Wang Alice S , Campos Jessica K , Colby Geoffrey P , Coon Alexander L , Lin Li-Mei 
Published: March 2020

BackgroundFlow modulation is the newest endovascular technique for treatment of cerebral aneurysms.ObjectiveTo investigate changes in aneurysm treatment practice patterns in the USA.MethodsFrom the 2007 to 2016, the National Inpatient Sample databases, hospital discharges associated with unruptured aneurysms (UA), and/or ruptured aneurysms (RA) having undergone surgical clipping (SC) and/or endovascular treatments (EVT) were identified using the International Classification of Diseases codes. Patient demographics, hospital characteristics, and clinical outcomes were reviewed. Five year subgroup analyses were performed for treatment differences.ResultsA total of 39 282 hospital discharges were identified with a significant increase in EVT (UA: SC n=7847 vs EVT n=12 797, p<0.001; RA: SC n=8108 vs EVT n=10 530, p<0.001). Hospitals in the South demonstrated the most significant EVT use regardless of aneurysm status (UA: SC n=258.5±53.6 vs EVT n=480.7±155.8, p<0.001; RA: SC n=285.6±54.3 vs EVT n=393.3±102.9, p=0.003). From 2007 to 2011, there was no significant difference in the mean number of cases for the treatment modalities (UA: SC n=847.4±107.7 vs EVT n=1120.4±254.1, p=0.21; RA: SC n=949.4±52.8 vs EVT n=1054.4±219.6, p=0.85). Comparatively, from 2012 to 2016, significantly more UA and RA were treated endovascularly (UA: SC n=722.0±43.4 vs EVT n=1439.0±419.2, p<0.001; RA: SC n=672.2±61.4 vs EVT n=1051.6±330.2, p=0.02).ConclusionsAs technological innovations continue to advance the neuroendovascular space, the standard of care for treatment of cerebral aneurysms is shifting further towards endovascular therapies over open surgical approaches in the USA.
Preparation of stable biopolymer composite suspension with metal/metal-oxide nanoparticles
Authors: Shi Shih-Chen , Yang Jason Hsiao Chun 
Published: March 2020

Hydroxypropyl methylcellulose (HPMC) is a kind of biopolymer that is biodegradable, environmentally friendly and possesses exceptional mechanical and tribological properties. Therefore, it could be used as a suitable alternative to plastic. However, HPMC deforms easily when subjected to loads, causing higher real contact area and adhesive force between HPMC and grinding counter. Therefore, HPMC films are easily damaged because of adhesive wear, which negatively affects wear resistance. Hence, nanoparticles (NPs) of Al, Cu, Al2O3 and CuO have been used as fillers to increase the wear resistance of the HPMC composite films. The uniform dispersion of NPs in the suspension is the most important factor, which is greatly related to the wear resistance after film formation. Nanosuspensions with various dispersant concentrations were prepared, and mixed with the HPMC solution to prepare composite solutions and composite films. The results showed that Span 80 could provide steric stabilization, and that it dispersed the NPs effectively in suspension. After mixing the suspension with the HPMC solution, the solution became more stable.
Platelets Disseminate Extracellular Vesicles in Lymph in Rheumatoid Arthritis
Authors: Tessandier Nicolas , Melki Imene , Cloutier Nathalie , Allaeys Isabelle , Miszta Adam , Tan Sisareuth , Milasan Andreea , Michel Sara , Benmoussa Abderrahim , Lévesque Tania , Côté Francine , McKenzie Steven E. , Gilbert Caroline , Provost Patrick , Brisson Alain R. , Wolberg Alisa S. , Fortin Paul R. , Martel Catherine , Boilard Éric 
Published: March 2020

Objective:
The lymphatic system is a circulatory system that unidirectionally drains the interstitial tissue fluid back to blood circulation. Although lymph is utilized by leukocytes for immune surveillance, it remains inaccessible to platelets and erythrocytes. Activated cells release submicron extracellular vesicles (EV) that transport molecules from the donor cell. In rheumatoid arthritis, EV accumulate in the joint where they can interact with numerous cellular lineages. However, whether EV can exit the inflamed tissue to recirculate is unknown. Here, we investigated whether vascular leakage that occurs during inflammation could favor EV access to the lymphatic system.

Approach and Results:

Using an in vivo model of autoimmune inflammatory arthritis, we show that there is an influx of platelet EV, but not EV from erythrocytes or leukocytes, in joint-draining lymph. In contrast to blood platelet EV, lymph platelet EV lacked mitochondrial organelles and failed to promote coagulation. Platelet EV influx in lymph was consistent with joint vascular leakage and implicated the fibrinogen receptor α2bβ
3
and platelet-derived serotonin.

Conclusions:
These findings show that platelets can disseminate their EV in fluid that is inaccessible to platelets and beyond the joint in this disease.
Sickle Cell Anemia Mediates Carotid Artery Expansive Remodeling That Can Be Prevented by Inhibition of JNK (c-Jun N-Terminal Kinase)
Authors: Song Hannah , Keegan Philip M. , Anbazhakan Suhaas , Rivera Christian P. , Feng Yundi , Omojola Victor O. , Clark Alexus A. , Cai Shuangyi , Selma Jada , Gleason Rudolph L. , Botchwey Edward A. , Huo Yunlong , Tan Wenchang , Platt Manu O. 
Published: March 2020

Objective:
Sickle cell anemia (SCA) causes chronic inflammation and multiorgan damage. Less understood are the arterial complications, most evident by increased strokes among children. Proteolytic mechanisms, biomechanical consequences, and pharmaceutical inhibitory strategies were studied in a mouse model to provide a platform for mechanistic and intervention studies of large artery damage due to sickle cell disease.

Approach and Results:
Townes humanized transgenic mouse model of SCA was used to test the hypothesis that elastic lamina and structural damage in carotid arteries increased with age and was accelerated in mice homozygous for SCA (sickle cell anemia homozygous genotype [SS]) due to inflammatory signaling pathways activating proteolytic enzymes. Elastic lamina fragmentation observed by 1 month in SS mice compared with heterozygous littermate controls (sickle cell trait heterozygous genotype [AS]). Positive immunostaining for cathepsin K, a powerful collagenase and elastase, confirmed accelerated proteolytic activity in SS carotids. Larger cross-sectional areas were quantified by magnetic resonance angiography and increased arterial compliance in SS carotids were also measured. Inhibiting JNK (c-jun N-terminal kinase) signaling with SP600125 significantly reduced cathepsin K expression, elastin fragmentation, and carotid artery perimeters in SS mice. By 5 months of age, continued medial thinning and collagen degradation was mitigated by treatment of SS mice with JNK inhibitor.

Conclusions:
Arterial remodeling due to SCA is mediated by JNK signaling, cathepsin proteolytic upregulation, and degradation of elastin and collagen. Demonstration in Townes mice establishes their utility for mechanistic studies of arterial vasculopathy, related complications, and therapeutic interventions for large artery damage due to SCA.
GFAP (Glial Fibrillary Acidic Protein)-Positive Progenitor Cells Contribute to the Development of Vascular Smooth Muscle Cells and Endothelial Cells—Brief Report
Authors: Osman Islam , Wang Liang , Hu Guoqing , Zheng Zeqi , Zhou Jiliang 
Published: March 2020

Objective:
While GFAP (glial fibrillary acidic protein) is commonly used as a classical marker for astrocytes in the central nervous system, GFAP-expressing progenitor cells give rise to other cell types during development. The goal of this study was to investigate whether GFAP-expressing progenitor cells contribute to the development of vascular cells in major arteries.

Approach and Results:

To label GFAP-expressing progenitor cells and their progeny, we crossed
GFAP
promoter-driven
Cre
recombinase mice (
GFAP
-
Cre
) with transgenic mice expressing the
Cre
-dependent
mTmG
dual fluorescent reporter gene. Using this genetic fate-mapping approach, here we demonstrate that GFAP-positive progenitor cells contribute to the development of vascular smooth muscle cells in both neural crest- and non-neural crest-derived vascular beds. In addition, GFAP-positive progenitor cells contribute to a subset of endothelial cells in some vasculature. Furthermore, fate-mapping analyses at multiple time points of mouse development demonstrate a time-dependent increase in the contribution of GFAP-positive progenitors to vascular smooth muscle cells, which mostly occurs in the postnatal period.

Conclusions:
Our study demonstrates that vascular smooth muscle cells and endothelial cells within the same vascular segment are developmentally heterogeneous, where varying proportions of vascular smooth muscle cells and endothelial cells are contributed by GFAP-positive progenitor cells.
Identification of a Plasma MicroRNA Profile Associated With Venous Thrombosis
Authors: Rodriguez-Rius Alba , Lopez Sonia , Martinez-Perez Angel , Souto Juan Carlos , Soria Jose Manuel 
Published: March 2020

Objective:
Venous thrombosis (VT) is a complex condition with a highly heritable genetic component that predisposes one to its development. Certain microRNAs (miRNAs) might be used as biomarkers of VT, but few studies have examined miRNA expression in this respect. The aim of the present work was to identify a plasma miRNA profile associated with VT.

Approach and Results:

miRNAs were analyzed by quantitative polymerase chain reaction in plasma samples from members of the GAIT-2 (Genetic Analysis of Idiopathic Thrombophilia 2) population (n=935). A discovery phase involving the screening of 752 miRNAs from a subset of 104 GAIT-2 subjects was followed by an internal validation phase in which the selected miRNAs were quantified in the whole GAIT-2 population. In the discovery phase, 16 miRNAs were selected, including 9 associated with VT and 7 that correlated with an intermediate phenotype of VT. In the next phase, 4 miRNAs were validated as differentially expressed (false discovery rate, <0.1) in VT: hsa-miR-126-3p, hsa-miR-885-5p, hsa-miR-194-5p, and hsa-miR-192-5p. The 4 miRNAs each returned a significant (
P
<0.05) odds ratio for VT (range of 1.3–1.8). A risk model including the 4 miRNAs, age, and sex returned an area under the receiver operating characteristic curve of 0.77. Moreover, all 4 miRNAs showed significant correlations with intermediate phenotypes of VT (eg, protein S and factor VII). The targets of the miRNAs in the blood coagulation pathway and their interactions are also discussed.

Conclusions:
The present results suggest a 4-miRNA plasma profile associated with VT is of potential use in predicting the risk of this condition.
Endothelium-Targeted Deletion of microRNA-15a/16-1 Promotes Poststroke Angiogenesis and Improves Long-Term Neurological Recovery
Authors: Sun Ping , Zhang Kai , Hassan Sulaiman H. , Zhang Xuejing , Tang Xuelian , Pu Hongjian , Stetler R. Anne , Chen Jun , Yin Ke-Jie 
Published: March 2020

Rationale:
Angiogenesis promotes neurological recovery after stroke and is associated with longer survival of stroke patients. Cerebral angiogenesis is tightly controlled by certain microRNAs (miRs), such as the miR-15a/16-1 cluster, among others. However, the function of the miR-15a/16-1 cluster in endothelium on postischemic cerebral angiogenesis is not known.

Objective:
To investigate the functional significance and molecular mechanism of endothelial miR-15a/16-1 cluster on angiogenesis in the ischemic brain.

Methods and Results:
Endothelial cell-selective miR-15a/16-1 conditional knockout (EC-miR-15a/16-1 cKO) mice and wild-type littermate controls were subjected to 1 hour middle cerebral artery occlusion followed by 28-day reperfusion. Deletion of miR-15a/16-1 cluster in endothelium attenuates post-stroke brain infarction and atrophy and improves the long-term sensorimotor and cognitive recovery against ischemic stroke. Endothelium-targeted deletion of the miR-15a/16-1 cluster also enhances post-stroke angiogenesis by promoting vascular remodeling and stimulating the generation of newly formed functional vessels, and increases the ipsilateral cerebral blood flow. Endothelial cell-selective deletion of the miR-15a/16-1 cluster up-regulated the protein expression of pro-angiogenic factors VEGFA (vascular endothelial growth factor), FGF2 (fibroblast growth factor 2), and their receptors VEGFR2 (vascular endothelial growth factor receptor 2) and FGFR1 (fibroblast growth factor receptor 1) after ischemic stroke. Consistently, lentiviral knockdown of the miR-15a/16-1 cluster in primary mouse or human brain microvascular endothelial cell cultures enhanced in vitro angiogenesis and up-regulated pro-angiogenic proteins expression after oxygen-glucose deprivation, whereas lentiviral overexpression of the miR-15a/16-1 cluster suppressed in vitro angiogenesis and down-regulated pro-angiogenic proteins expression. Mechanistically, miR-15a/16-1 translationally represses pro-angiogenic factors VEGFA, FGF2, and their receptors VEGFR2 and FGFR1, respectively, by directly binding to the complementary sequences within 3′-untranslated regions of those messenger RNAs.

Conclusions:
Endothelial miR-15a/16-1 cluster is a negative regulator for postischemic cerebral angiogenesis and long-term neurological recovery. Inhibition of miR-15a/16-1 function in cerebrovascular endothelium may be a legitimate therapeutic approach for stroke recovery.
Reactivation of the Epicardium at the Origin of Myocardial Fibro-Fatty Infiltration During the Atrial Cardiomyopathy
Authors: Suffee Nadine , Moore-Morris Thomas , Jagla Bernd , Mougenot Nathalie , Dilanian Gilles , Berthet Myriam , Proukhnitzky Julie , Le Prince Pascal , Tregouet David A. , Pucéat Michel , Hatem Stéphane N. 
Published: March 2020

Rationale:
Fibro-fatty infiltration of subepicardial layers of the atrial wall has been shown to contribute to the substrate of atrial fibrillation.

Objective:
Here, we examined if the epicardium that contains multipotent cells is involved in this remodeling process.

Methods and Results:

One hundred nine human surgical right atrial specimens were evaluated. There was a relatively greater extent of epicardial thickening and dense fibro-fatty infiltrates in atrial tissue sections from patients aged over 70 years who had mitral valve disease or atrial fibrillation when compared with patients aged less than 70 years with ischemic cardiomyopathy as indicated using logistic regression adjusted for age and gender. Cells coexpressing markers of epicardial progenitors and fibroblasts were detected in fibro-fatty infiltrates. Such epicardial remodeling was reproduced in an experimental model of atrial cardiomyopathy in rat and in Wilms tumor 1 (WT1)
CreERT2/+
;ROSA-tdT
+/−
mice. In the latter, genetic lineage tracing demonstrated the epicardial origin of fibroblasts within fibro-fatty infiltrates. A subpopulation of human adult epicardial-derived cells expressing PDGFR (platelet-derived growth factor receptor)-α were isolated and differentiated into myofibroblasts in the presence of Ang II (angiotensin II). Furthermore, single-cell RNA-sequencing analysis identified several clusters of adult epicardial-derived cells and revealed their specification from adipogenic to fibrogenic cells in the rat model of atrial cardiomyopathy.

Conclusions:
Epicardium is reactivated during the formation of the atrial cardiomyopathy. Subsets of adult epicardial-derived cells, preprogrammed towards a specific cell fate, contribute to fibro-fatty infiltration of subepicardium of diseased atria. Our study reveals the biological basis for chronic atrial myocardial remodeling that paves the way of atrial fibrillation.