Estimation of the Oxidative Deterioration of Turbine Oil Using Membrane Patch Color

Lubricating oils degrade into two main products: oxidation products and solid particles. Oxidation products, called varnish, of turbine oils for power generation have become a particularly serious problem in recent years. The first step in determining the potential to produce varnish is to determine the remaining life of the antioxidant in the oil, but even though turbine oil may have antioxidants of sufficient longevity, varnish problems still occur frequently. Accordingly, to prevent varnish, it is necessary to diagnose oil oxidation products. Thus, the authors have developed a diagnostic method using membrane patch color, but the relationship between membrane patch color and the remaining life of turbine oils has yet to be clarified. This paper investigates a new method for estimating the oxidative degradation of turbine oils that uses membrane patch color and the dry turbine oxidation stability test (dry TOST) based on oxidation products and the remaining life of the turbine oils. Sample oils were prepared and degraded by oxidation in the laboratory using a dry TOST apparatus, and the membrane patch color was measured using a colorimetric patch analyzer (CPA). The relationship between membrane patch color and the rotating pressure vessel oxidation test (RPVOT) residual rate was then investigated. The results show that the new estimation method using the CPA and dry TOST is able to monitor the decrease of the RPVOT residual rate from the early stages of oxidative deterioration

Effect of Acoustic Emission Sensor Location on the Detection of Grinding Wheel Deterioration in Cylindrical Grinding

The acoustic emission (AE) technique is an effective method for monitoring grinding wheels, and numerous studies have been published on applying an AE to monitor grinding wheels. However, there are few studies on the effect of the location of the AE sensor in stably acquiring the AE signals generated during deterioration in cylindrical grinding wheels. In this study, we propose a stable method for detecting the deterioration of a cubic boron nitride (cBN) grinding wheel during cylindrical grinding using AE. We compared the AE signals acquired during grinding from an AE sensor located on the hydrostatic bearing, which supports the grinding wheel shaft, with those from the tailstock spindle. Although positioning the AE sensor on the hydrostatic bearing was found to reduce the AE signal intensity, the AE signal variations were smaller at the same grinding position, and the effect of the grinding position was less than that for the tailstock spindle. Moreover, positioning an AE sensor on the hydrostatic bearing is considered to provide the characteristics of AE signals specifically focused on the changes in cBN on the grinding wheel surface allowing the surface roughness of the workpiece to be estimated during grinding

SMAP2 Regulates Retrograde Transport from Recycling Endosomes to the Golgi

<div><p>Retrograde transport is where proteins and lipids are transported back from the plasma membrane (PM) and endosomes to the Golgi, and crucial for a diverse range of cellular functions. Recycling endosomes (REs) serve as a sorting station for the retrograde transport and we recently identified evection-2, an RE protein with a pleckstrin homology (PH) domain, as an essential factor of this pathway. How evection-2 regulates retrograde transport from REs to the Golgi is not well understood. Here, we report that evection-2 binds to SMAP2, an Arf GTPase-activating protein. Endogenous SMAP2 localized mostly in REs and to a lesser extent, the trans-Golgi network (TGN). SMAP2 binds evection-2, and the RE localization of SMAP2 was abolished in cells depleted of evection-2. Knockdown of SMAP2, like that of evection-2, impaired the retrograde transport of cholera toxin B subunit (CTxB) from REs. These findings suggest that evection-2 recruits SMAP2 to REs, thereby regulating the retrograde transport of CTxB from REs to the Golgi.</p> </div

Co-localization analysis of SMAP2 with several RE/TGN proteins.

<p>COS-1 cells were fixed with TCA, permeabilized, and then stained for SMAP2 (green) and the indicated proteins (red). For evection-2, Myc-tagged evection-2 was transiently expressed and stained with anti-Myc antibody. For CTxB, cells were pulsed for 3 min with Alexa 594-CTxB, chased for 35 min at 37°C, and fixed. Fluorescence intensity profile along white dotted lines is shown in the right column. Blue lines in the graph indicate regions where SMAP2 do not co-localize with TfnR or TGN46. Pearson coefficient was obtained using multiple images (n > 12 cells). Data represent mean ± SD. Scale bars, 1 µm.</p

SMAP2 interacts with evection-2.

<p>(A) Flag-tagged evection-2 was expressed in COS-1 cells for 24 h. The cell homogenates were treated with 0 or 0.1 mM DSP and then solubilized by adding 1% Triton X-100. The lysates were then immunoprecipitated with anti-FLAG antibody. Immunoprecipitates were separated by SDS-PAGE, and then blotted with anti-FLAG, anti-SMAP2, anti-GP73, or anti-β-actin antibody. A 50-kDa band observed in the β-actin blot was IgG heavy chain. (B) Cells treated with control siRNA or evection-2 siRNA for 48 h were fixed, permeabilized, and stained for SMAP2 and Rab11. Nuclei were stained with DAPI (blue). Scale bars, 10 µm. (C) Pearson coefficient between SMAP2 and Rab11 in (B). Data represent mean ± SD, n > 16 cells. ***P < 0.001, Student’s two-tailed <i>t</i> test.</p

Knockdown of SMAP2 impaired the retrograde transport of CTxB from REs.

<p>(A) Cells treated with control siRNA (left column) or SMAP2 siRNA#1 (right column) were pulsed for 3 min at 37°C with Alexa594-CTxB and chased for the indicated times. Cells were then fixed, permeabilized, and stained for GM130. Nuclei were stained with DAPI (blue). (B) Cells in (A) were examined visually if CTxB reached the Golgi. The percentage of cells in which CTxB reached the Golgi after a 60-min chase was shown. Data represent mean ± SD, n > 150 cells. *P < 0.05, **P < 0.01, ***P < 0.001, Student’s two-tailed <i>t</i> test. (C) Cells treated with control or SMAP2 siRNA#1 were pulsed for 5 min at 37°C with Alexa488-Tfn and chased for the indicated times. Cells were then fixed, permeabilized, and stained for GM130. Nuclei were stained with DAPI (blue). (D) Cells in (C) were examined visually if Tfn was in REs. The percentage of cells in which Tfn was in REs at the indicated times was shown. Data represent mean ± SD, n > 70 cells. ns, not significant, Student’s two-tailed <i>t</i> test. Scale bars, 10 µm.</p

RE localization of endogenous SMAP2.

<p>COS-1 cells were fixed with TCA, permeabilized, and then stained for SMAP2 (green) and the indicated organelle markers (red). Nuclei were stained with DAPI (blue). Magnified images of boxed areas around the perinulcear region are shown in the right column. Scale bars, 10 µm.</p

Long-term safety and efficacy of patisiran for hereditary transthyretin-mediated amyloidosis with polyneuropathy: 12-month results of an open-label extension study

© 2020 Elsevier Ltd. All rights reserved.Background: Hereditary transthyretin-mediated amyloidosis is a rare, inherited, progressive disease caused by mutations in the transthyretin (TTR) gene. We assessed the safety and efficacy of long-term treatment with patisiran, an RNA interference therapeutic that inhibits TTR production, in patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy. Methods: This multicentre, open-label extension (OLE) trial enrolled patients at 43 hospitals or clinical centres in 19 countries as of Sept 24, 2018. Patients were eligible if they had completed the phase 3 APOLLO or phase 2 OLE parent studies and tolerated the study drug. Eligible patients from APOLLO (patisiran and placebo groups) and the phase 2 OLE (patisiran group) studies enrolled in this global OLE trial and received patisiran 0·3 mg/kg by intravenous infusion every 3 weeks with plans to continue to do so for up to 5 years. Efficacy assessments included measures of polyneuropathy (modified Neuropathy Impairment Score +7 [mNIS+7]), quality of life, autonomic symptoms, nutritional status, disability, ambulation status, motor function, and cardiac stress, with analysis by study groups (APOLLO-placebo, APOLLO-patisiran, phase 2 OLE patisiran) based on allocation in the parent trial. The global OLE is ongoing with no new enrolment, and current findings are based on the interim analysis of the patients who had completed 12-month efficacy assessments as of the data cutoff. Safety analyses included all patients who received one or more dose of patisiran up to the data cutoff. This study is registered with ClinicalTrials.gov, NCT02510261. Findings: Between July 13, 2015, and Aug 21, 2017, of 212 eligible patients, 211 were enrolled: 137 patients from the APOLLO-patisiran group, 49 from the APOLLO-placebo group, and 25 from the phase 2 OLE patisiran group. At the data cutoff on Sept 24, 2018, 126 (92%) of 137 patients from the APOLLO-patisiran group, 38 (78%) of 49 from the APOLLO-placebo group, and 25 (100%) of 25 from the phase 2 OLE patisiran group had completed 12-month assessments. At 12 months, improvements in mNIS+7 with patisiran were sustained from parent study baseline with treatment in the global OLE (APOLLO-patisiran mean change -4·0, 95 % CI -7·7 to -0·3; phase 2 OLE patisiran -4·7, -11·9 to 2·4). Mean mNIS+7 score improved from global OLE enrolment in the APOLLO-placebo group (mean change from global OLE enrolment -1·4, 95% CI -6·2 to 3·5). Overall, 204 (97%) of 211 patients reported adverse events, 82 (39%) reported serious adverse events, and there were 23 (11%) deaths. Serious adverse events were more frequent in the APOLLO-placebo group (28 [57%] of 49) than in the APOLLO-patisiran (48 [35%] of 137) or phase 2 OLE patisiran (six [24%] of 25) groups. The most common treatment-related adverse event was mild or moderate infusion-related reactions. The frequency of deaths in the global OLE was higher in the APOLLO-placebo group (13 [27%] of 49), who had a higher disease burden than the APOLLO-patisiran (ten [7%] of 137) and phase 2 OLE patisiran (0 of 25) groups. Interpretation: In this interim 12-month analysis of the ongoing global OLE study, patisiran appeared to maintain efficacy with an acceptable safety profile in patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy. Continued long-term follow-up will be important for the overall assessment of safety and efficacy with patisiran.info:eu-repo/semantics/publishedVersio