3rd Loop Research Articles

Stability performance of series coupled natural circulation system with different operating procedures

Series coupled natural circulation system with the last loop being an open-air loop finds application as an infinite mission time passive decay heat removal system in nuclear power plants and solar thermal systems. Hence the stability behavior of series coupled rectangular loops with horizontal heater and horizontal cooler orientation was experimentally studied. The loop was subjected to various operating procedures viz., start up from rest, power raising from a stable steady state and power step down from an unstable state to witness that the stability threshold was not a unique value, thus confirming the existence of a hysteresis phenomenon. The stability threshold enhancement of the system with orifice plates was maximum for the lowest orifice diameter. The coupled system was chosen with an unstable first loop and the instability was found to transmit from loop#1 to the subsequent loops. However, the oscillation amplitude was highly attenuated and seemed to be nearly stable in the 2nd and 3rd loop without any flow reversals even when the first loop was unstable with chaotic bidirectional pulsing. In case of bi-directional pulsing in loop#1, the heat exchanger between the first two loops operated alternatively in co-current and counter-current mode with no change in the flow direction of loop#2. A delay in the flow initiation was found for start-up from rest, which increased from the first loop to the last loop and decreased with the increase in power input. Further, the numerical simulation with the one-dimensional model reproduced the oscillatory behavior in loop#1, with the predicted stability threshold being considerably lower compared to the experiments. The attenuation of the oscillations in the loop#2 as observed in the experiments could be reproduced. Predicted transients showed practically no oscillations in loop#3 corroborating the experimental observations. The attenuation of the oscillations in loop#2 and the absence of oscillations in loop#3 were attributed to the damping caused by the wall and also due to the higher Lt/D ratio in loop#2 and a vertical air flow channel in loop#3 respectively. The phase plots indicated a near periodic oscillation compared to the highly chaotic pattern in the experiments, presumably due to the higher power at which instability was observed in the experiments. The deviations were also due to the secondary flows being generated in the large diameter loop as the simulation was based on 1D along with the heat loss being neglected.

Effects of Copper Extraction-Stripping Loops on Entrainment in Aqueous Raffinate

Effects of extraction-stripping loops of organic phase on organic chemical entrainment in the aqueous raffinate in copper solvent extraction were studied in this paper. Results demonstrated that the total amount of organic chemicals lost in the aqueous raffinate decreased with the increase of times of extraction-stripping loops but reached largest at third loop. Entrainment was the dominate way of organic chemicals losing in the aqueous raffinate at early stage of the loops. The formation of entrainment and its stabilization mechanism was also studied. The average size of entrained droplet trended to increase with extraction-stripping loops increasing. Meanwhile, the absolute value of zeta potential trended to decrease. The surface tension of the aqueous raffinate increased after reaching the minimum value 41.3 mN/m at the 3rd loop. It showed that the formation of entrained droplets and its stability were mainly affected by the surface tension of aqueous raffinate.

Identification of amino acids in human colipase that mediate adsorption to lipid emulsions and mixed micelles

The adsorption of colipase is essential for pancreatic triglyceride lipase activity and efficient dietary fat digestion. Yet, little is known about which specific amino acids in the hydrophobic surface of colipase influence adsorption. In this study, we systematically substituted alanine or tryptophan at residues implicated in adsorption of colipase to an interface. We expressed, purified recombinant colipase mutants and characterized the ability of each alanine mutant to restore activity to lipase in the presence of bile salts. The functions of L16A, Y55A, I79A and F84A colipase were most impaired with activities ranging from 20 to 60% of wild-type colipase. We next characterized the fluorescence properties of the tryptophan mutants in the absence and presence of bile–salt–oleic acid mixed micelles. We performed steady-state emission spectra to determine peak shift and I330/I350 ratio and acrylamide quenching curves to characterize the environment of the residues. The analysis supports a model of adsorption that includes residues Leu 34 and Leu 36 on the 2nd loop, Tyr 55 and Tyr 59 on the 3rd loop and Ile 75 and Ile 79 on the 4th loop. The analysis confirms that Phe 84 is not part of the adsorption surface and likely stabilizes the conformation of colipase. Contrary to the predictions of computer modeling, the results provide strong support for an essential role of Tyr 55 in colipase adsorption to mixed micelles. The results indicate that the adsorption of colipase to mixed micelles is mediated by specific residues residing in a defined surface of colipase.

Pathogenic role of anti-M3 muscarinic acetylcholine receptor immune response in Sjögren's syndrome

M3 muscarinic acetylcholine receptor (M3R) is expressed in exocrine glands (e.g., salivary glands [SGs] and lachrymal glands), and plays a crucial role in exocrine secretion. M3R reactive T cells have been detected in circulating mononuclear cells of 40% of patients with Sjögren's syndrome (SS), and the major T cell epitopes of M3R in those patients with HLA-DR B1×0901 are located in the second loop of M3R. Moreover, autoantibodies (autoAbs) against M3R are also present in sera of around 50% of patients with SS, and several B cell epitopes, such as N-region, 1st, 2nd, and 3rd loop of M3R, have been identified. Functional analysis using human SG cell lines showed that autoAbs against the 2nd loop of M3R suppressed intracellular Ca(2+) influx, suggesting inhibition of saliva secretion. To clarify whether the M3R reactive immune response induces autoimmune sialadenitis (AIS), M3R(-/-) mice were immunized with M3R synthetic peptides and their splenocytes transferred into Rag1(-/-) mice. The recipients developed severe sialadenitis, and cell transfer studies indicated that T cells are key factors in the pathogenesis of AIS. These results indicate that the M3R immune reaction plays a key pathogenic role in AIS, suggesting that M3R molecule acts as an autoantigen in the pathogenesis of SS.

3P038 ロドプシン細胞内第3ループと機能的に相同な、ファミリー2 : G蛋白質共役型受容体の細胞内ループの探索(蛋白質(構造・構造機能相関),ポスター発表,第45回日本生物物理学会年会)

3P038 ロドプシン細胞内第3ループと機能的に相同な、ファミリー2 : G蛋白質共役型受容体の細胞内ループの探索(蛋白質(構造・構造機能相関),ポスター発表,第45回日本生物物理学会年会)

Invagination intestinale aiguë de cause inhabituelle: Hyperplasie hétérotopique pseudo-tumorale des glandes de brunner

We report the first case of small-bowel intussusception caused by a tumour-like Brunner's gland hyperplasia in a 26 year old woman. The patient presented with intense abdominal pain. Abdominal and pelvic contrast enhanced CT-scan suggested small bowel intussusception involving the first jejunal loop. A 15 cm long polypoid mass was found in the jejunumectomy specimen (2nd and 3rd loops). Histological examination revealed Brunner's gland hyperplasia in the jejunal mucosa and submucosa. Considering the jejunal location of the lesion, it must be considered malformative and heterotopic Brunner's gland hyperplasia.

The Role of Phosphorylation in D1 Dopamine Receptor Desensitization: EVIDENCE FOR A NOVEL MECHANISM OF ARRESTIN ASSOCIATION

Homologous desensitization of D(1) dopamine receptors is thought to occur through their phosphorylation leading to arrestin association which interdicts G protein coupling. In order to identify the relevant domains of receptor phosphorylation, and to determine how this leads to arrestin association, we created a series of mutated D(1) receptor constructs. In one mutant, all of the serine/threonine residues within the 3rd cytoplasmic domain were altered (3rdTOT). A second construct was created in which only three of these serines (serines 256, 258, and 259) were mutated (3rd234). We also created four truncation mutants of the carboxyl terminus (T347, T369, T394, and T404). All of these constructs were comparable with the wild-type receptor with respect to expression and adenylyl cyclase activation. In contrast, both of the 3rd loop mutants exhibited attenuated agonist-induced receptor phosphorylation that was correlated with an impaired desensitization response. Sequential truncation of the carboxyl terminus of the receptor resulted in a sequential loss of agonist-induced phosphorylation. No phosphorylation was observed with the most severely truncated T347 mutant. Surprisingly, all of the truncated receptors exhibited normal desensitization. The ability of the receptor constructs to promote arrestin association was evaluated using arrestin-green fluorescent protein translocation assays and confocal fluorescence microscopy. The 3rd234 mutant receptor was impaired in its ability to induce arrrestin translocation, whereas the T347 mutant was comparable with wild type. Our data suggest a model in which arrestin directly associates with the activated 3rd cytoplasmic domain in an agonist-dependent fashion; however, under basal conditions, this is sterically prevented by the carboxyl terminus of the receptor. Receptor activation promotes the sequential phosphorylation of residues, first within the carboxyl terminus and then the 3rd cytoplasmic loop, thereby dissociating these domains and allowing arrestin to bind to the activated 3rd loop. Thus, the role of receptor phosphorylation is to allow access of arrestin to its receptor binding domain rather than to create an arrestin binding site per se.

The middle portion in the second cytoplasmic loop of the thyrotropin receptor plays a crucial role in adenylate cyclase activation.

We have examined the role of the 2nd cytoplasmic loop of the TSH receptor (TSHR) in TSH- and TSHR autoantibody-stimulated cAMP and inositol phosphate formation using mutants created by substituting sequences from the alpha 1- or beta 2-adrenergic receptors (AR). Unlike similar substitution mutants involving the 3rd cytoplasmic loop that lose agonist-induced inositol phosphate but not cAMP increase after transfection into Cos-7 cells, mutants involving the 2nd loop showed significant change in generating both signals. Mutant B525, which substitutes residues 525-527 with a comparable beta 2-AR sequence, exhibited a complete loss in TSH- or Graves' immunoglobulin G-increased cAMP signaling and a lesser loss in phosphoinositide signaling. This is a unique mutant in which cAMP response was completely lost in all those involving the 2nd or 3rd cytoplasmic loop. On the other hand, mutant B528, in which residues 528-532 are substituted with a comparable beta 2-AR sequence, exhibited the most profound loss in phosphoinositide signaling. Mutants involving portions surrounding residues 528-532 in the 2nd cytoplasmic loop had milder losses in agonist-increased phosphoinositide signaling and much lesser losses in agonist-increased cAMP generation. The transfection efficiency of all transfectants was the same. All transfectants with mutant or wild type TSHR had a similar amount and identical profile of TSHR mRNA in Northern blots and TSHR forms on Western blots. Thus, the 2nd cytoplasmic loop is important for agonist-induced cAMP as well as for phosphoinositide signal generation, whereas the 3rd loop appears to be important only for the latter. The most important determinant for agonist-increased cAMP signal generation is in the middle of the 2nd loop, around residues 525-527. In contrast, the determinants most critical for agonist-induced phosphoinositide signaling are also located in the middle of the 2nd loop, around residues 528-532, and those with less importance are broadly distributed.