Evaluation of amine emissions from the post-combustion CO2 capture pilot plant

AbstractIn this work, we evaluated amine emissions from 10ton-CO2/day scale pilot plant in Mikawa Power Plant of Sigma Power Co. Ltd. within TS-1 solvent. Firstly, we investigated that how sampling gas flow rate affects measured value of amine concentration in flue gas by using on-line sampling method with PTR-MS analyzer. It was found that the error from an iso-kinetic sampling rises sharply for lower sampling velocities and in the range of higher sample stream velocities, however the error is lower. Secondly, we compared between beginning of operation and 2,800hours operation in terms of amine emissions at Mikawa pilot plant under one set of conditions. At beginning of operation, there were no degraded amines in TS-1 solution. Thus, there were no amine emissions of degraded amines. However, at 2,800hours operating, in addition to TS-1 emissions, some quantity of emissions of degraded amines were detected even though degraded amines were much less than TS-1 main amine in TS-1 solution. Toshiba improved operating conditions such as plant system, water wash system to reduce the amount of amine emissions. As a result, the latest tests showed lower emissions of less than 1 ppm(v/v) at 2,800hours operation. A concentration of degraded amine [D] in TS-1 solution at 2,800hours operation, which was nearly detection limit, was lower than other degraded amines. Nevertheless, degraded amine [D] accounted for the greater part of amine emissions after water wash was improved. This result suggested that it is crucial to reduce the volatility of emitted degraded amines in order to improve performance of suppression amine emissions further. Then, finally we evaluated effect of addition acid to reduce the volatility of degraded amine [D]. The results in diluted aqueous amines at 40°C showed that effectiveness of acid for reducing amine volatility is in the order: sulfuric acid > oxalic acid carbonic acid produced by 10%CO2 > boric acid

A tri-axial accelerometer with structure-based voltage operation by using series-connected piezoelectric elements

AbstractOutput-voltage operation on a sensor structure is proposed and a tri-axial accelerometer with low cross-axis sensitivities is designed. The output voltage between the electrodes sandwiching piezoelectric thin-films on a deforming structure is proportional to the in-plane stress of the piezoelectric thin-film. If the piezoelectric thin-film is processed to separated elements and the electrodes of the elements are connected in series, the output voltages from the series-connected piezoelectric elements are multiplied or canceled depending on the situations of the internal-stresses (i.e. compressive or tensile) of the elements. Proper design of the electrode connections by taking the deformation shape of structures into consideration can realize expected outputvoltage operations on the device structure. The principle of structure-based output-voltage operation is applied to the design of a tri-axial accelerometer with low cross-axes sensitivities. Finite-element-method (FEM) simulations of the tri-axial accelerometer revealed the cross-axis sensitivity of less than 1.5%

Effects of NADPH oxidase inhibitor in diabetic nephropathy

Effects of NADPH oxidase inhibitor in diabetic nephropathy.BackgroundWe used apocynin to test the hypothesis that superoxide anion (O−2) from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase underlies the development of diabetic nephropathy in the rat.MethodsRats received apocynin (16 mg/kg/day) from 2 to 8 weeks after inducing diabetes mellitus (DM) with streptozotocin.ResultsDM increased excretion of hydrogen peroxide (H2O2), lipid peroxidation products (LPO), nitric oxide products (NOx), and protein. The kidneys of rats with DM had increased expression of p47phox and gp91phox and endothelial nitric oxide synthase (eNOS), and increased mesangial matrix with expression of fibronectin and collagen I. Apocynin prevented the increase in excretion of H2O2, LPO, and protein in diabetic rats, increased renal NOx generation, and prevented the increased renal expression of gp91phox and the membrane fraction of p47phox, and reverted the mesangial matrix expansion.ConclusionActivation of NADPH oxidase with translocation of p47phox to the membrane underlies the oxidative stress and limited NO generation, despite enhanced eNOS expression in a model of diabetic nephropathy. Apocynin prevents these changes and the associated proteinuria

Penetration of the sigmoid colon to the posterior uterine wall secondary to diverticulitis: a case report

<p>Abstract</p> <p>Introduction</p> <p>Penetration of the colon to the posterior uterine wall secondary to diverticulitis is unusual, with diagnostic methods not yet established. Non-invasive imaging, such as computed tomography and magnetic resonance imaging may help to establish a proper diagnosis, but confirmation may be reached only after surgical exploration.</p> <p>Case presentation</p> <p>We report the case of a 78-year-old Japanese woman who presented with a low grade fever and mild diarrhea which occurred two or three times a week. Computed tomography and magnetic resonance imaging demonstrated a capsular lesion including an air structure with a diameter of 5 cm, between the posterior aspect of the uterine body and the sigmoid colon. A gastrograffin enema and colonoscopy demonstrated a giant diverticulum of the sigmoid colon with no evidence of malignancy. These data confirmed the diagnosis of diverticulitis complicated by a giant diverticulum. Because of a relapsing fever after therapy with antibiotics, the patient had en bloc surgical treatment of the uterus, fallopian tubes, ovaries and sigmoid colon, the organs involved in the diverticulitis, followed by an uneventful recovery.</p> <p>Conclusion</p> <p>This is a rare case report of penetration of the sigmoid colon to the posterior uterine wall secondary to diverticulitis.</p

The Toll-like Receptor Protein Rp105 Regulates Lipopolysaccharide Signaling in B Cells

The susceptibility to infections induced by Gram-negative bacteria is largely determined by innate immune responses to bacteria cell wall lipopolysaccharide (LPS). The stimulation of B cells by LPS enhances their antigen-presenting capacity and is accompanied by B cell proliferation and secretion of large quantities of LPS-neutralizing antibodies. Similar to macrophages and neutrophils, the LPS-induced activation of B cells is dependent on Toll-like receptor (TLR)4. Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans. The analysis of mice homozygous for the null mutation in the RP105 gene revealed impaired proliferative and humoral immune responses of RP105-deficient B cells to LPS. Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor κB activation. These data suggest the existence of the TLR4–RP105 signaling module in the LPS-induced B cell activation

Transgenic Monkey Model of the Polyglutamine Diseases Recapitulating Progressive Neurological Symptoms

Age-associated neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and the polyglutamine (polyQ) diseases, are becoming prevalent as a consequence of elongation of the human lifespan. Although various rodent models have been developed to study and overcome these diseases, they have limitations in their translational research utility owing to differences from humans in brain structure and function and in drug metabolism. Here, we generated a transgenic marmoset model of the polyQ diseases, showing progressive neurological symptoms including motor impairment. Seven transgenic marmosets were produced by lentiviral introduction of the human ataxin 3 gene with 120 CAG repeats encoding an expanded polyQ stretch. Although all offspring showed no neurological symptoms at birth, three marmosets with higher transgene expression developed neurological symptoms of varying degrees at 3–4 months after birth, followed by gradual decreases in body weight gain, spontaneous activity, and grip strength, indicating time-dependent disease progression. Pathological examinations revealed neurodegeneration and intranuclear polyQ protein inclusions accompanied by gliosis, which recapitulate the neuropathological features of polyQ disease patients. Consistent with neuronal loss in the cerebellum, brain MRI analyses in one living symptomatic marmoset detected enlargement of the fourth ventricle, which suggests cerebellar atrophy. Notably, successful germline transgene transmission was confirmed in the second-generation offspring derived from the symptomatic transgenic marmoset gamete. Because the accumulation of abnormal proteins is a shared pathomechanism among various neurodegenerative diseases, we suggest that this new marmoset model will contribute toward elucidating the pathomechanisms of and developing clinically applicable therapies for neurodegenerative diseases.ArticleeNeuro.4(2):e0250(2017)journal articl

Structural basis for Ccd1 auto-inhibition in the Wnt pathway through homomerization of the DIX domain

Wnt signaling plays an important role in governing cell fate decisions. Coiled-coil-DIX1 (Ccd1), Dishevelled (Dvl), and Axin are signaling proteins that regulate the canonical pathway by controlling the stability of a key signal transducer β-catenin. These proteins contain the DIX domain with a ubiquitin-like fold, which mediates their interaction in the β-catenin destruction complex through dynamic head-to-tail polymerization. Despite high sequence similarities, mammalian Ccd1 shows weaker stimulation of β-catenin transcriptional activity compared with zebrafish (z) Ccd1 in cultured cells. Here, we show that the mouse (m) Ccd1 DIX domain displays weaker ability for homopolymerization than that of zCcd1. Furthermore, X-ray crystallographic analysis of mCcd1 and zCcd1 DIX domains revealed that mCcd1 was assembled into a double-helical filament by the insertion of the β1-β2 loop into the head-to-tail interface, whereas zCcd1 formed a typical single-helical polymer similar to Dvl1 and Axin. The mutation in the contact interface of mCcd1 double-helical polymer changed the hydrodynamic properties of mCcd1 so that it acquired the ability to induce Wnt-specific transcriptional activity similar to zCcd1. These findings suggest a novel regulatory mechanism by which mCcd1 modulates Wnt signaling through auto-inhibition of dynamic head-to-tail homopolymerization