bluuebunny/crossref_metadata_2025_split huggingface dataset:
Laboratory Investigation of Low-Tension-Gas Flooding for Improved Oil Recovery in Tight Formations
Authors: Szlendak S.M.. M. , Nguyen N.. , Nguyen Q.P.. P. 
Published: August 2013

Summary
This paper establishes low-tension gas (LTG) as a method for submiscible tertiary recovery in tight sandstone and carbonate reservoirs. The LTG process involves the use of surfactant and gas to mobilize and then displace residual crude after waterflood at a greatly reduced oil/water interfacial tension (IFT). This method allows extending surfactant enhanced oil recovery (EOR) in sub-20-md formations in which polymer is impractical because of plugging, shear, or the requirement to use a low-molecular-weight polymer.
The proposed strategy is tested through the coinjection of nitrogen and a slug/drive surfactant solution. Results indicate favorable mobilization and displacement of residual crude oil in both tight-carbonate and tight-sandstone reservoirs. Tertiary recovery of 75−90% of residual oil in place (ROIP) was achieved for cores with 2- to 15-md permeability. High LTG tertiary recovery is contrasted with results from reference surfactant (no gas) flooding (28% ROIP tertiary recovery) and immiscible gas coinjection (no surfactant) flooding (13% ROIP tertiary recovery). In addition, high initial oil saturation was tested to determine the process tolerance to oil and to evaluate the potential for application during secondary recovery. Under such conditions, this method achieved a recovery of 84% of oil originally in place (OOIP), suggesting the potential application of this process at secondary recovery.
To better understand the physical mechanisms that affect mobilization and displacement, the early production of an elongated oil bank at reduced fractional flow of oil was shown to be an attribute of high crude-oil relative mobility and low pore volume (PV) available to mobile oil. This should favorably affect economics during chemical flooding by accelerating the production of an oil bank. Next, by application of salinity as a conservative tracer and oil material balance, gas saturation during LTG floods was calculated to be 18 to 22%. By comparing effluent salinity profiles across floods, a qualitative understanding of in-situ fluid dispersion associated with macroscopic displacement stability is developed. The results indicate that in-situ foaming was present, which enabled mobility control, and that stable displacement of in-situ fluids was achieved during flooding.
Expandable Solid-Steel Liner Applications in the Marcellus
Authors: Cameron J. R. , Cooper B. S. , Gusevik R. T. 
Published: August 2013

Abstract
In the Marcellus Shale gas play in Pennsylvania and West Virginia, solid-steel expandable liners have been used over the last three years to restore casing damaged by over-pressuring during completion operations and to cover unwanted perforations to enable hydraulic fracturing. This paper describes the technology of expandable solid-steel liners and presents representative case histories in the Marcellus Shale.
Solid-steel expandable liners are expanded downhole using a pressure-driven cone that enlarges the diameter of the liner by permanently deforming it beyond its yield point but not to failure. While expanding the liner, elastomeric seals on the outside are compressed against the base casing to provide pressure integrity and anchoring.
In the Marcellus Shale, one well experienced a casing split in the lateral section during the primary cement job, and in a second well, a casing split occurred in the lateral section while pressuring open the toe fracturing sleeve. In a third well, three sets of squeeze perforations over a 1,300-ft interval had to be covered. In a fourth well, circulation for a cement job could not be established requiring the lateral liner to be perforated over its entire length in order to squeeze cement behind the casing. All of these wells required restorations of 5-1/2-in. 20 lb/ft casing to enable hydraulic fracturing.
In the first well, the casing split was repaired using a standard single-joint of expandable liner allowing the fracturing treatment to be performed using controlled screenouts (sand plugs) for fracturing-stage diversion below the expandable liner. In the second well, the casing split was repaired using two standard joints of expandable liner and the fracturing treatment was performed using drillable composite fracturing plugs (frac plugs) set below the installed liner for fracturing-stage diversion. In the third well, three separate high-performance single joints of expandable liner were used to cover the three sets of squeeze perforations over the 1,300-ft interval to enable fracturing using frac plugs set below the three single-joint expandable liners. In the fourth well, the entire lateral was relined with the solid-steel expandable liner, maintaining inside diameter (ID) sufficient for fracturing with frac plugs set inside the liner. In all these shale gas wells, solid-steel expandable liners provided reliable and robust solutions enabling fracturing to proceed as planned.
A Workflow to Evaluate Porosity, Mineralogy, and TOC in the Utica-Point Pleasant Shale Play
Authors: Murphy Eric , Warner Matthew , Sarmah Bhaskar 
Published: August 2013

Abstract
Porosity is a key reservoir property used in petrophysical evaluations. Obtaining realistic porosity estimates in unconventional reservoirs is challenging using only conventional logs. Conventional log porosity measurements are affected by the presence of kerogen in organic-rich reservoirs. Techniques such as ΔLogR can be used to predict total organic carbon (TOC) which can be converted to kerogen volume. The kerogen volume can then be used to apply corrections to conventional porosity measurements. However, these techniques require prior knowledge of thermal maturity or core measurements such as vitrinite reflectance (Ro).
The predicted TOC can also be used in conjunction with geochemical elemental measurements for a more accurate assessment of formation kerogen and mineralogy, as well as for hydrocarbon volumes. Nuclear magnetic resonance (NMR) logs measure only the fluids present and represent a total porosity unaffected by solid components such as kerogen and bitumen. Recent observations in numerous unconventional resource plays indicate that NMR log porosity provides the best match to core porosity and does not require corrections for kerogen. NMR log porosity is available in real time as an input to the petrophysical model long before core measurements can be completed. The complex refractive index method (CRIM) in conjunction with mineralogy log data can be used to compute accurate dielectric porosities, which exclude both kerogen and hydrocarbon. Integrating core TOC, predicted TOC, mineral analysis, NMR, and dielectric information, a final verification of the kerogen volume, porosity, hydrocarbon content, and mineral analysis can be assessed.
Based on previous work in the Eagle Ford Shale, a comprehensive workflow was developed for unconventional source rock reservoir interpretation. The workflow integrates conventional logs, a geochemical log, an NMR log, and a dielectric log to predict TOC, kerogen volume, mineralogy, total porosity, and hydrocarbon volume. This paper will show results from the Eagle Ford wells upon which this workflow is based. Then, we apply the workflow to the Utica-Point Pleasant Shale Play and compare those results to core measurements.
Physicochemical fractionation of americium, thorium, and uranium in Chernozem soil after sharp temperature change and soil drought
Authors: Kovacheva Petya , Mitsiev Svilen , Djingova Rumyana 
Published: August 2013

AbstractA sequential extraction procedure was used to study the changes in the physicochemical forms of americium (Am), thorium (Th), and uranium (U) in laboratory-contaminated Chernozem soil as a result of sharp variations of the environmental temperature and soil moisture. The influence of freezing and soil drought on the radio-ecological hazard was evaluated three months after radioactive contamination with aqueous solutions of 241Am, 234Th, and U. The subsequent changes in the physicochemical forms of the actinides, caused by sharp increases in the environmental temperature and soil moisture, were examined for one month. The data showed that continuous freezing increased the potentially mobile forms of Am and Th but had the opposite effect on U. Prolonged soil drought did not influence the fractionation of Am and Th but led to the redistribution of U between the carbonates and organic matter and caused its immobilisation. The sharp increase in the temperature of the frozen soil caused the immobilisation of Am and Th and increased the potential mobility of U. The warming and enhanced humidity of the dry soil led to the immobilisation of Am and redistribution of U between the soil phases.
Characterization of Resident B Cells of Vascular Walls in Human Atherosclerotic Patients
Authors: Hamze Moustafa , Desmetz Caroline , Berthe Marie Laurence , Roger Pascal , Boulle Nathalie , Brancherau Pascal , Picard Eric , Guzman Caroline , Tolza Claire , Guglielmi Paul 
Published: August 2013

Abstract
Animal models of atherosclerosis suggest that B cells have contradictory protective or proatherogenic effects that are also subset and context dependent. To further understand the pathophysiology of human atheroma, we characterized local Ig production and functional properties of resident B cells in human arterial lesions. Ig repertoires were analyzed by RT-PCR in carotid endarterectomy samples. Cytokine, differentiation marker and transcription factor mRNA expression was studied on arterial wall lymphocytes isolated by laser capture microdissection. Ig sequence analysis revealed that individual samples each contained a limited number of B cell clones. Functional α and γ mRNAs made up the majority of H chain mRNAs in the adventitia. Clonal evolution of Ig V regions, expression of activation-induced cytidine deaminase, clonal H chain switch, and an inverted λ/κ ratio of Ig L chain usage indicated that a local differentiation process was taking place in arterial walls. Clonotypic markers revealed different plaque and adventitia Ig repertoires and a B cell recirculation between adventitia and draining lymph nodes. Microdissected mononuclear cells had an activated phenotype expressing IL-6, GM-CSF, and TNF-α, whereas IL-2, IL-4, IL-10, M-CSF, and IFN-γ were not detected. Adventitial oligoclonal resident B cells of atherosclerotic patients are mainly mature B2 (conventional) CD20− plasmablasts lacking markers of terminal differentiation to plasma cell (CD138 and Blimp-1). They present hallmarks of Ag-driven maturation and could act on inflammation and disease progression directly or by promoting polarization of other immune cells.
IDO1 Plays an Immunosuppressive Role in 2,4,6-Trinitrobenzene Sulfate–Induced Colitis in Mice
Authors: Takamatsu Manabu , Hirata Akihiro , Ohtaki Hirofumi , Hoshi Masato , Hatano Yuichiro , Tomita Hiroyuki , Kuno Toshiya , Saito Kuniaki , Hara Akira 
Published: August 2013

Abstract
IDO, an enzyme that degrades the essential amino acid l-tryptophan to N-formylkynurenine, is known to exert immunomodulatory effects in a number of diseases and disorders. IDO expression is increased in tumors, where it is thought to be involved in tumor evasion by suppressing the immune response. A competitive inhibitor of IDO is currently being tested in clinical trials for relapsed or refractory solid tumors; however, there remains a concern that attenuation of the immunosuppressive function of IDO might exacerbate inflammatory responses. In this study, we investigated the role of IDO in 2,4,6-trinitrobenzene sulfate (TNBS)–induced colitis in mice by gene deletion and pharmacological inhibition. TNBS treatment induced significantly more severe colitis in Ido1 gene–deficient (Ido1−/−) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Consistent with this, the expression of Ido1 was increased in the colonic interstitial tissues of TNBS-treated Ido1+/+ mice. Furthermore, transplantation of Ido1+/+ bone marrow cells into Ido1−/− mice reduced the pathological damage associated with colitis, altered the expression of cytokines, including IFN-γ, TNF-α, and IL-10, and increased the number of CD4+ Foxp3+ regulatory T cells in the colon. Pharmacological inhibition of IDO enzymatic activity by oral administration of 1-methyltryptophan (1-methyl-l-tryptophan or 1-methyl-d-tryptophan) significantly increased the severity of TNBS-induced colitis in mice, demonstrating that both stereoisomers can promote colitis. Collectively, our data indicate that IDO1 plays an important immunoregulatory role in the colon.
Establishment of a Human Allergy Model Using Human IL-3/GM-CSF–Transgenic NOG Mice
Authors: Ito Ryoji , Takahashi Takeshi , Katano Ikumi , Kawai Kenji , Kamisako Tsutomu , Ogura Tomoyuki , Ida-Tanaka Miyuki , Suemizu Hiroshi , Nunomura Satoshi , Ra Chisei , Mori Akio , Aiso Sadakazu , Ito Mamoru 
Published: August 2013

Abstract
The development of animal models that mimic human allergic responses is crucial to study the pathophysiology of disease and to generate new therapeutic methodologies. Humanized mice reconstituted with human immune systems are essential to study human immune reactions in vivo and are expected to be useful for studying human allergies. However, application of this technology to the study of human allergies has been limited, largely because of the poor development of human myeloid cells, especially granulocytes and mast cells, which are responsible for mediating allergic diseases, in conventional humanized mice. In this study, we developed a novel transgenic (Tg) strain, NOD/Shi-scid-IL2rγnull (NOG), bearing human IL-3 and GM-CSF genes (NOG IL-3/GM–Tg). In this strain, a large number of human myeloid cells of various lineages developed after transplantation of human CD34+ hematopoietic stem cells. Notably, mature basophils and mast cells expressing FcεRI were markedly increased. These humanized NOG IL-3/GM–Tg mice developed passive cutaneous anaphylaxis reactions when administered anti–4-hydroxy-3-nitrophenylacetyl IgE Abs and 4-hydroxy-3-nitrophenylacetyl. More importantly, a combination of serum from Japanese cedar pollinosis patients and cedar pollen extract also elicited strong passive cutaneous anaphylaxis responses in mice. Thus, to our knowledge, our NOG IL-3/GM–Tg mice are the first humanized mouse model to enable the study of human allergic responses in vivo and are excellent tools for preclinical studies of allergic diseases.
Innate Immune Cell–Derived Microparticles Facilitate Hepatocarcinoma Metastasis by Transferring Integrin αMβ2 to Tumor Cells
Authors: Ma Jingwei , Cai Wenqian , Zhang Yi , Huang Chunmei , Zhang Huafeng , Liu Jing , Tang Ke , Xu Pingwei , Katirai Foad , Zhang Jianmin , He Wei , Ye Duyun , Shen Guan-Xin , Huang Bo 
Published: August 2013

Abstract
Mechanisms by which tumor cells metastasize to distant organs still remain enigmatic. Immune cells have been assumed to be the root of metastasis by their fusing with tumor cells. This fusion theory, although interpreting tumor metastasis analogically and intriguingly, is arguable to date. We show in this study an alternative explanation by immune cell–derived microparticles (MPs). Upon stimulation by PMA or tumor cell–derived supernatants, immune cells released membrane-based MPs, which were taken up by H22 tumor cells, leading to tumor cell migration in vitro and metastasis in vivo. The underlying molecular basis was involved in integrin αMβ2 (CD11b/CD18), which could be effectively relayed from stimulated innate immune cells to MPs, then to tumor cells. Blocking either CD11b or CD18 led to significant decreases in MP-mediated tumor cell metastasis. This MP-mediated transfer of immune phenotype to tumor cells might also occur in vivo. These findings suggest that tumor cells may usurp innate immune cell phenotypes via MP pathway for their metastasis, providing new insight into tumor metastatic mechanism.
Persistence of the Bacterial Pathogen Granulibacter bethesdensis in Chronic Granulomatous Disease Monocytes and Macrophages Lacking a Functional NADPH Oxidase
Authors: Chu Jessica , Song Helen H. , Zarember Kol A. , Mills Teresa A. , Gallin John I. 
Published: August 2013

Abstract
Granulibacter bethesdensis is a Gram-negative pathogen in patients with chronic granulomatous disease (CGD), a deficiency in the phagocyte NADPH oxidase. Repeated isolation of genetically identical strains from the same patient over years, and prolonged waxing and waning seropositivity in some subjects, raises the possibility of long-term persistence. G. bethesdensis resists killing by serum, CGD polymorphonuclear leukocytes (PMN), and antimicrobial peptides, indicating resistance to nonoxidative killing mechanisms. Although G. bethesdensis extends the survival of PMN, persistent intracellular bacterial survival might rely on longer-lived macrophages and their precursor monocytes. Therefore, we examined phagocytic killing by primary human monocytes and monocyte-derived macrophages (MDM). Cells from both normal and CGD subjects internalized G. bethesdensis similarly. G. bethesdensis stimulated superoxide production in normal monocytes, but to a lesser degree than in normal PMN. Normal but not CGD monocytes and MDM killed G. bethesdensis and required in vitro treatment with IFN-γ to maintain this killing effect. Although in vitro IFN-γ did not enhance G. bethesdensis killing in CGD monocytes, it restricted growth in proportion to CGD PMN residual superoxide production, providing a potential method to identify patients responsive to IFN-γ therapy. In IFN-γ–treated CGD MDM, G. bethesdensis persisted for the duration of the study (7 d) without decreasing viability of the host cells. These results indicate that G. bethesdensis is highly resistant to oxygen-independent microbicides of myeloid cells, requires an intact NADPH oxidase for clearance, and can persist long-term in CGD mononuclear phagocytes, most likely relating to the persistence of this microorganism in infected CGD patients.
Human Airway Eosinophils Exhibit Preferential Reduction in STAT Signaling Capacity and Increased CISH Expression
Authors: Burnham Mandy E. , Koziol-White Cynthia J. , Esnault Stephane , Bates Mary E. , Evans Michael D. , Bertics Paul J. , Denlinger Loren C. 
Published: August 2013

AbstractAllergic asthma, a chronic respiratory disorder marked by inflammation and recurrent airflow obstruction, is associated with elevated levels of IL-5 family cytokines and elevated numbers of eosinophils (EOS). IL-5 family cytokines elongate peripheral blood EOS (EOSPB) viability, recruit EOSPB to the airways, and, at higher concentrations, induce degranulation and reactive oxygen species generation. Although airway EOS (EOSA) remain signal ready in that GM-CSF treatment induces degranulation, treatment of EOSA with IL-5 family cytokines no longer confers a survival advantage. Because the IL-5 family receptors have common signaling capacity, but are uncoupled from EOSA survival, whereas other IL-5 family induced endpoints remain functional, we tested the hypothesis that EOSA possess a JAK/STAT-specific regulatory mechanism (because JAK/STAT signaling is critical to EOS survival). We found that IL-5 family–induced STAT3 and STAT5 phosphorylation is attenuated in EOSA relative to blood EOS from airway allergen–challenged donors. However, IL-5 family–induced ERK1/2 phosphorylation is not altered between EOSA and EOS from airway allergen–challenged donors. These observations suggest EOSA possess a regulatory mechanism for suppressing STAT signaling distinct from ERK1/2 activation. Furthermore, we found, in EOSPB, IL-5 family cytokines induce members of the suppressors of cytokine signaling (SOCS) genes, CISH and SOCS1. Additionally, following allergen challenge, EOSA express significantly more CISH and SOCS1 mRNA and CISH protein than EOSPB counterparts. In EOSPB, long-term pretreatment with IL-5 family cytokines, to varying degrees, attenuates IL-5 family–induced STAT5 phosphorylation. These data support a model in which IL-5 family cytokines trigger a selective downregulation mechanism in EOSA for JAK/STAT pathways.
Resident Renal Mononuclear Phagocytes Comprise Five Discrete Populations with Distinct Phenotypes and Functions
Authors: Kawakami Takahisa , Lichtnekert Julia , Thompson Lucas J. , Karna Prasanthi , Bouabe Hicham , Hohl Tobias M. , Heinecke Jay W. , Ziegler Steven F. , Nelson Peter J. , Duffield Jeremy S. 
Published: August 2013

Abstract
Recent reports have highlighted greater complexity, plasticity, and functional diversity of mononuclear phagocytes (MPCs), including monocytes, macrophages, and dendritic cells (DCs), in our organs than previously understood. The functions and origins of MPCs resident within healthy organs, especially in the kidney, are less well understood, whereas studies suggest they play roles in disease states distinct from recruited monocytes. We developed an unbiased approach using flow cytometry to analyze MPCs residing in the normal mouse kidney, and identified five discrete subpopulations according to CD11b/CD11c expression as well as F4/80, CD103, CD14, CD16, and CD64 expression. In addition to distinct marker profiles, these subpopulations have different lineages and expression of genes involved in tissue homeostasis, including angiogenesis. Among them, the CD11bintCD11cint F4/80high subpopulation notably exhibited high capacity to produce a representative anti-inflammatory cytokine, IL-10. Each subpopulation had different degrees of both macrophage (phagocytosis) and DC (Ag presentation) capacities, with a tendency to promote differentiation of regulatory T cells, whereas two of these showed expression of transcription factors reported to be highly expressed by classical DCs, and proclivity to exit the kidney following stimulation with LPS. In summary, resident kidney MPCs comprise discrete subpopulations, which cannot be simply classified into the conventional entities, and they produce anti-inflammatory and tissue-homeostatic factors to differing degrees.
Th17 Cells Carrying TCR Recognizing Epidermal Autoantigen Induce Psoriasis-like Skin Inflammation
Authors: Nishimoto Shuhei , Kotani Hitoshi , Tsuruta Sanae , Shimizu Nana , Ito Minako , Shichita Takashi , Morita Rimpei , Takahashi Hayato , Amagai Masayuki , Yoshimura Akihiko 
Published: August 2013

Abstract
Psoriasis is considered a Th17-type autoimmune skin inflammatory disease; however, involvement of an autoantigen-specific TCR has not been established. In this study, we show that psoriasis-like skin inflammation can be induced by autoreactive Th17 cells. We previously developed the desmoglein 3–specific TCR-transgenic (Dsg3H1) mouse, in which CD4+ T cells recognize physiological epidermal autoantigen. T cells from Dsg3H1 mice were polarized into Th17 cells in vitro and then adoptively transferred into Rag2−/− mice. Dsg3H1-Th17 cells induced severe psoriasis-like skin inflammation within 2 wk after transfer in the tissues in which desmoglein 3 is expressed. Such pathology was not observed when wild-type Th17 cells or Th1-skewed Dsg3H1 T cells were transferred, and it was strongly suppressed by anti–IL-12/23 and anti–IL-17 Abs. Although IFN-γ+/IL-17+ T cells accumulated in the skin lesions of mice that received Dsg3H1-Th17 cells, IFN-γ–deficient Dsg3H1-Th17 cells were fully pathogenic. These results demonstrate that cutaneous psoriasis-like immunopathology can be developed by epidermis-specific recognition of Th17 cells, which is strictly dependent on IL-17 but not IFN-γ.