Search

We report on the synergic effect of surfactants and chelating agents on the mechanism to remove stubborn keratin grime (keratin-Ca), which is bound with calcium ions and one of the most difficult grimes to remove, in order to make it easier to clean bathtubs in less time and with less scrubbing. Our approach was to focus on keratin swelling, which we achieved by applying aqueous solutions with chelating agents and anionic surfactants, the combination of which greatly improved the swelling ratio, resulting in quick, easy removal of keratin-Ca with water rinsing and little scrubbing. For the swelling process, we added chelating agents and anionic surfactants to swell the keratin-Ca by both capturing calcium ions and improving solution permeation. Furthermore, we measured the structural change of the keratin-Ca during swelling by TD-NMR and confirmed that a certain combination of chelating agent and anionic surfactant improved swelling by affecting not only the amorphous part such as the keratin matrix, but also the crystalline part such as the intermediate filaments (IFs). [ABSTRACT FROM AUTHOR]

ADOC, Abu Dhabi Oil Co., Ltd. (Japan), marks another historical milestone with the commencement of oil production from a new oil field in November 2017. ADOC was established in 1968, and since then has been conducting stable operations through utilization of the best production technology that fully copes with the environment protection rules and regulations. The new oil field was granted as an additional oil field to its existing three oil fields when ADOC renewed its concession agreement in December 2012. Soon after the renewal of the concession, ADOC launched the new oil field development activities. The development plan of the field consisted of; 3D seismic acquisition, subsurface studies, drilling of appraisal wells and production wells, dredging of a channel and construction of the new artificial island and surface facilities. This paper will summarize the various challenges of field development in an environmentally sensitive area and the measures that were implemented. [ABSTRACT FROM AUTHOR]

ADOC, Abu Dhabi Oil Co., Ltd. (Japan), has been operating three oil fields offshore Abu Dhabi for more than 45 years. Recently, ADOC developed and commenced production from an oil field located in a Marine Protected Area, an area designated as a Biosphere Reserve by the UNESCO Secretariat. Therefore, special environmental measures were considered for the development of the field. The development plan of the field consisted of; 3D seismic acquisition, subsurface studies, zero discharge operations, dredging of a channel and construction of artificial island and surface facilities. This paper will summarize the various challenges of field development in an environmentally sensitive area, the measures that were implemented and the lessons learnt. [ABSTRACT FROM AUTHOR]

Murine membrane-bound phospholipase A2 receptor 1 (PLA2R) is shed and released into plasma in a soluble form that retains all of the extracellular domains. Relatively little is known about human PLA2R. This study examined whether human soluble PLA2R has biological functions and whether soluble PLA2R exists in human plasma. Here, we showed that human recombinant soluble PLA2R (rsPLA2R) bound to collagen-I and inhibited interaction of collagen-I with the extracellular domain of integrin 1 on the cell surface of human embryonic kidney 293 (HEK293) cells. As a result, rsPLA2R suppressed integrin 1-mediated migratory responses of HEK293 cells to collagen-I in Boyden chamber experiments. Inhibition of phosphorylation of FAK Tyr397 was also observed. Similar results were obtained with experiments using soluble PLA2R released from HEK293 cells transfected with a construct encoding human soluble PLA2R. rsPLA2R lacking the fibronectin-like type II (FNII) domain had no inhibitory effects on cell responses to collagen-I, suggesting an important role of the FNII domain in the interaction of rsPLA2R with collagen-I. In addition, rsPLA2R suppressed the migratory response to collagen-IV and binding of collagen-IV to the cell surface of human podocytes that endogenously express membranebound, full-length PLA2R. Immunoprecipitation and Western blotting showed the existence of immunoreactive PLA2R in human plasma. In conclusion, human recombinant soluble PLA2R inhibits integrin 1- mediated cell responses to collagens. Further studies are warranted to elucidate whether immunoreactive PLA2R in human plasma has the same properties as rsPLA2R. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are increased in ischemic tissues and necessary for revascularization; however, the mechanism remains unclear. Exposure of cysteine residues to ROS in the presence of glutathione (GSH) generates GSH-protein adducts that are specifically reversed by the cytosolic thioltransferase, glutaredoxin-1 (Glrx). Here, we show that a key angiogenic transcriptional factor hypoxiainducible factor (HIF)-1α is stabilized by GSH adducts, and the genetic deletion of Glrx improves ischemic revascularization. In mouse muscle C2C12 cells, HIF-1α protein levels are increased by increasing GSH adducts with cell-permeable oxidized GSH (GSSG-ethyl ester) or 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanyl thiocarbonylamino) phenylthiocarbamoylsulfanyl] propionic acid (2-AAPA), an inhibitor of glutathione reductase. A biotin switch assay shows that GSSG-ester-induced HIF-1α contains reversibly modified thiols, and MS confirms GSH adducts on Cys520 (mouse Cys533). In addition, an HIF-1α Cys520 serine mutant is resistant to 2-AAPA-induced HIF-1α stabilization. Furthermore, Glrx overexpression prevents HIF-1α stabilization, whereas Glrx ablation by siRNA increases HIF-1α protein and expression of downstream angiogenic genes. Blood flow recovery after femoral artery ligation is significantly improved in Glrx KO mice, associated with increased levels of GSH-protein adducts, capillary density, vascular endothelial growth factor (VEGF)-A, and HIF- 1α in the ischemic muscles. Therefore, Glrx ablation stabilizes HIF-1α by increasing GSH adducts on Cys520 promoting in vivo HIF-1α stabilization, VEGF-A production, and revascularization in the ischemic muscles. [ABSTRACT FROM AUTHOR]

The role of stromal cell-derived factor-1α (SDF-1α) expressed in infarcted myocardium is unknown in humans. We examined whether SDF-1α produced in an infarcted myocardial lesion may play a role in left ventricle (LV) remodeling and dysfunction in patients with acute myocardial infarction (AMI). We measured SDF-1α levels in plasma obtained from aortic root (AO) and anterior interventricular vein (AIV) in the early phase (2 wk after MI) and the chronic phase (6 mo after MI) in 80 patients with anterior MI. An increment in SDF-1α level from AO to AIV, reflecting SDF-1α release from infarcted myocardium, was more frequent in patients with MI in the early phase of MI [n = 52 (65%), P = 0.03] but not in the chronic phase of MI [n = 46 (58%), P = 0.11] compared with that in control patients [n = 6/17 (35%)]. On linear regression analysis, the transmyocardial gradient in SDF-1α level in the chronic phase of MI was correlated with percentage changes in LV end-diastolic volume index (r = 0.39, P < 0.001), LV end-systolic volume index (r = 0.38, P < 0.001), and LV ejection fraction (r = -0.26, P = 0.01) 6 mo after AMI. By contrast, the transmyocardial gradient of SDF-1α in the early phase of MI had no significant correlations. In conclusion, the production of SDF-1α in infarcted myocardium in the chronic phase of MI was associated with LV adverse remodeling and progressive dysfunction in AMI survivors. [ABSTRACT FROM AUTHOR]

Copyright of Proceedings of the Estonian Academy of Sciences is the property of Teaduste Akadeemia Kirjastus and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Group IV A cytosolic phospholipase A2 (cPLA2α), which preferentially cleaves arachidonic acid from phospholipids, plays a role in apoptosis and tissue injury. Downstream signals in response to tumor necrosis factor (TNF)-α, a mediator of myocardial ischemia-reperfusion (I/R) injury, involve cPLA2α activation. This study examined the potential role of cPLA2α and its mechanistic link with TNF-α in myocardial I/R injury using cPLA2α knockout (cPLA2α-/-) mice. Myocardial I/R was created with 10-wk-old male mice by 1 h ligation of the left anterior descending coronary artery, followed by 24 h of reperfusion. As a result, compared with wild-type (cPLA2α+/+) mice, cPLA2α-/- mice had a 47% decrease in myocardial infarct size, preservation of echocardiographic left ventricle (LV) function (%fractional shortening: 14 vs. 21%, respectively), and lower content of leukotriene B4 and thromboxane B2 (62 and 50% lower, respectively) in the ischemic myocardium after I/R. Treatment with the TNF-α inhibitor (soluble TNF receptor II/IgG1 Fc fusion protein, sTNFR:Fc) decreased myocardial I/R injury and LV dysfunction in cPLA2α+/+ mice but not cPLA2α-/- mice. sTNFR:Fc also suppressed cPLA2α phosphorylation in the ischemic myocardium after I/R of cPLA2α+/+ mice. Similarly, sTNFR:Fc exerted protective effects against hypoxia-reoxygenation (H/R)-induced injury in the cultured cardiomyocytes from cPLA2α+/+ mice but not cPLA2α-/- cardiomyocytes. H/R and TNF-α induced cPLA2α phosphorylation in cPLA2α+/+ cardiomyocytes, which was reversible by sTNFR:Fc. In cPLA2α-/- cardiomyocytes, TNF-α induced apoptosis and release of arachidonic acid to a lesser extent than in cPLA2α+/+ cardiomyocytes. In conclusion, disruption of cPLA2α attenuates myocardial I/R injury partly through inhibition of TNF-α-mediated pathways. [ABSTRACT FROM AUTHOR]

Group X secretory PLA2 (sPLA2-X) is expressed in neutrophils and plays a role in the pathogenesis of neutrophil-mediated tissue inflammation and injury. This study tested the hypothesis that sPLA2-X in neutrophils may contribute to the pathogenesis of abdominal aortic aneurysms (AAA) using sPLA2-X-/- mice. AAA was created by application of CaCl2 to external surface of aorta. As a result, the aortas of sPLA2- X-/- mice had smaller diameters (percent increase from baseline; 24.8 ± 3.5% vs. 49.9 ± 9.1%, respectively; P < 0.01), a reduced grade of elastin degradation, and lower activities of elastase and gelatinase (26% and 19% lower, respectively) after CaCl2 treatment compared with sPLA2-X+/+ mice. In sPLA2-X-/- mice, immunofluorescence microscopic images showed that the immunoreactivity of sPLA2-X was detected only in neutrophils within aortic walls 3 days, 1, 2, and 6 wk after CaCl2 treatment, whereas the immunoreactivity was not detected in macrophages or mast cells in aortic walls. sPLA2-X immunoreactivity also was colocalized in cells expressing matrix metalloproteinase (MMP)-9. Neutrophils isolated from sPLA2- X-/- mice had lower activities of elastase, gelatinase, and MMP-9 in response to stimuli compared with sPLA2-X+/+ mice. The attenuated release of elastase and gelatinase from sPLA2-X-/- neutrophils was reversed by exogenous addition of mouse sPLA2-X protein. The adoptive transfer of sPLA2-X+/+ neutrophils days 0 and 3 after CaCl2 treatment reversed aortic diameters and elastin degradation grades in the lethally irradiated sPLA2-X+/+ mice reconstituted with sPLA2- X-/- bone marrow to an extent similar to that seen in sPLA2-X+/+ mice. In conclusion, sPLA2-X in neutrophils plays a pathogenic role in AAA in a mice model. [ABSTRACT FROM AUTHOR]

Abstract  We report a 48-year-old woman with primary diffuse leptomeningeal gliomatosis (PDLG) histologically diagnosed as gliosarcoma. She was admitted complaining of headache, numbness of the right arm, double vision, and visual field defects. Computerized tomography (CT) scans showed ventricular dilatation consistent with communicating hydrocephalus. Magnetic resonance imaging (MRI) revealed diffuse meningeal thickening and gadolinium enhancement without a definite intraparenchymal lesion. Whole-spine MRI demonstrated across-the-board dural thickening and gadolinium enhancement. Cytological examination showed atypical anaplastic cells. As no diagnosis could be made she underwent biopsy of the leptomeninges. Histological examination of the specimen returned a diagnosis of gliosarcoma. Despite chemotherapy and radiotherapy she died 11 months after admission. Autopsy findings included gliosarcoma in the leptomeninges and spinal cord without an underlying parenchymal tumor. To our knowledge, this is the first report of primary diffuse leptomeningeal gliosarcomatosis. [ABSTRACT FROM AUTHOR]