142 research outputs found

    Fouling substances causing variable rejection of a small and uncharged trace organic chemical by reverse osmosis membranes

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    The safety of recycled water for potable water reuse can be enhanced by improving the reliability of reverse osmosis (RO) treatment for the removal of trace organic chemicals. This study assessed the mechanisms underlying the variable rejection of a carcinogenic N-nitrosamine, namely N-nitrosodimethylamine (NDMA), caused by RO membrane fouling. Foulants that cause the variable rejection were evaluated through rejection tests and foulant characterization. The RO treatment of wastewaters with and without pre-treatment using an ultrafiltration or nanofiltration membrane showed that NDMA rejection commonly increased with increasing membrane fouling. The characterization of organics in the treated wastewater samples revealed that increased NDMA rejection can be caused by foulants composed of low-molecular-weight organics (<300 Da), including tryptophan (or tryptophan-like substances). It is speculated that small organics such as tryptophan form a densely packed cake layer on the membrane surface, which may function as an additional barrier for the membrane transport of NDMA. The results of this study indicate that RO membrane fouling that occurs during long-term wastewater treatment can increase NDMA rejection. The enhanced separation performance can yield positive consequences for the credibility of RO treatment in potable water reuse

    Noninvasive assessment of left and right ventricular filling in myocardial infarction with a two-dimensional Doppler echocardiography method

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    Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery.Three measurements were performed from the trans-mitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: 1) acceleration half-time, 2) deceleration half-time of early diastolic rapid inflow, and 3) the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction.Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV. Impaired diastolic filling of the right ventricle compensated by enhanced right atrial contraction was revealed in groups I, II and III. It is supposed that myocardial damage of the interventricular septum and a part of the right ventricular anterior wall perfused from the left anterior descending branch might be one of the causes for mildly impaired diastolic filling of the right ventricle in group I patients with a patent right coronary artery

    Evaluation of internal margins for prostate for step and shoot intensity‐modulated radiation therapy and volumetric modulated arc therapy using different margin formulas

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    [Purpose] This feasibility study evaluated the intra-fractional prostate motion using an ultrasound image-guided system during step and shoot intensity-modulated radiation therapy (SS-IMRT) and volumetric modulated arc therapy (VMAT). Moreover, the internal margins (IMs) using different margin formulas were calculated. [Methods] Fourteen consecutive patients with prostate cancer who underwent SS-IMRT (n = 5) or VMAT (n = 9) between March 2019 and April 2020 were considered. The intra-fractional prostate motion was observed in the superior–inferior (SI), anterior–posterior (AP), and left–right (LR) directions. The displacement of the prostate was defined as the displacement from the initial position at the scanning start time, which was evaluated using the mean ± standard deviation (SD). IMs were calculated using the van Herk and restricted maximum likelihood (REML) formulas for SS-IMRT and VMAT. [Results] For SS-IMRT, the maximum displacements of the prostate motion were 0.17 ± 0.18, 0.56 ± 0.86, and 0.18 ± 0.59 mm in the SI, AP, and LR directions, respectively. For VMAT, the maximum displacements of the prostate motion were 0.19 ± 0.64, 0.22 ± 0.35, and 0.14 ± 0.37 mm in the SI, AP, and LR directions, respectively. The IMs obtained for SS-IMRT and VMAT were within 2.3 mm and 1.2 mm using the van Herk formula and within 1.2 mm and 0.8 mm using the REML formula. [Conclusions] This feasibility study confirmed that intra-fractional prostate motion was observed with SS-IMRT and VMAT using different margin formulas. The IMs should be determined according to each irradiation technique using the REML margin

    Calpain-dependent disruption of nucleo-cytoplasmic transport in ALS motor neurons

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    Nuclear dysfunction in motor neurons has been hypothesized to be a principal cause of amyotrophic lateral sclerosis (ALS) pathogenesis. Here, we investigated the mechanism by which the nuclear pore complex (NPC) is disrupted in dying motor neurons in a mechanistic ALS mouse model (adenosine deaminase acting on RNA 2 (ADAR2) conditional knockout (AR2) mice) and in ALS patients. We showed that nucleoporins (Nups) that constituted the NPC were cleaved by activated calpain via a Ca2+-permeable AMPA receptor-mediated mechanism in dying motor neurons lacking ADAR2 expression in AR2 mice. In these neurons, nucleo-cytoplasmic transport was disrupted, and the level of the transcript elongation enzyme RNA polymerase II phosphorylated at Ser2 was significantly decreased. Analogous changes were observed in motor neurons lacking ADAR2 immunoreactivity in sporadic ALS patients. Therefore, calpain-dependent NPC disruption may participate in ALS pathogenesis, and inhibiting Ca2+-mediated cell death signals may be a therapeutic strategy for ALS.UTokyo Research掲載「核と細胞質間の分子輸送経路の破綻が筋萎縮性側索硬化症に関与」 URI: http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/disruption-of-molecule-transport-pathway-between-nucleus-and-cytoplasm-involved-in-als.htmlUTokyo Research "Disruption of molecule transport pathway between nucleus and cytoplasm involved in ALS" URI: http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/disruption-of-molecule-transport-pathway-between-nucleus-and-cytoplasm-involved-in-als.htm

    Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus

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    Synchronous oscillations of thousands of cellular clocks in the suprachiasmatic nucleus (SCN), the circadian centre, are coordinated by precisely timed cell–cell communication, the principle of which is largely unknown. Here we show that the amount of RGS16 (regulator of G protein signalling 16), a protein known to inactivate Gαi, increases at a selective circadian time to allow time-dependent activation of intracellular cyclic AMP signalling in the SCN. Gene ablation of Rgs16 leads to the loss of circadian production of cAMP and as a result lengthens circadian period of behavioural rhythm. The temporally precise regulation of the cAMP signal by clock-controlled RGS16 is needed for the dorsomedial SCN to maintain a normal phase-relationship to the ventrolateral SCN. Thus, RGS16-dependent temporal regulation of intracellular G protein signalling coordinates the intercellular synchrony of SCN pacemaker neurons and thereby defines the 24 h rhythm in behaviour
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