坂口䙥子文学研究 [論文要旨及び審査の要旨]

関西大

Microscopic description of Gamow-Teller transitions in middle pf--shell nuclei by a realistic shell model calculation

GT transitions in $N=28\sim 30$ nuclei are studied in terms of a large-scale realistic shell-model calculation, by using Towner's microscopic parameters. $B({\rm GT})$ values to low-lying final states are reproduced with a reasonable accuracy. Several gross properties with respect to the GT transitions are investigated with this set of the wavefunctions and the operator. While the calculated total GT$^-$ strengths show no apparent disagreement with the measured ones, the calculated total GT$^+$ strengths are somewhat larger than those obtained from charge-exchange experiments. Concerning the Ikeda sum-rule, the proportionality of $S_{\rm GT}$ to $(N-Z)$ persists to an excellent approximation, with a quenching factor of 0.68. For the relative GT$^-$ strengths among possible isospin components, the lowest isospin component gathers greater fraction than expected by the squared CG coefficients of the isospin coupling. It turns out that these relative strengths are insensitive to the size of model space. Systematics of the summed $B({\rm GT})$ values are discussed for each isospin component.Comment: IOP-LaTeX 23 pages, to appear in J. Phys. G., 5 Postscript figures available upon reques

High density lipoprotein promotes proliferation of adipose-derived stem cells via S1P1 receptor and Akt, ERK1/2 signal pathways

Introduction: Adipose-derived stem cells (ADSC) are non-hematopoietic mesenchymal stem cells that have shown great promise in their ability to differentiate into multiple cell lineages. Their ubiquitous nature and the ease of harvesting have attracted the attention of many researchers, and they pose as an ideal candidate for applications in regenerative medicine. Several reports have demonstrated that transplanting ADSC can promote repair of injured tissue and angiogenesis in animal models. Survival of these cells after transplant remains a key limiting factor for the success of ADSC transplantation. Circulating factors like High Density Lipoprotein (HDL) has been known to promote survival of other stems cells like bone marrow derived stem cells and endothelial progenitor cells, both by proliferation and by inhibiting cell apoptosis. The effect of HDL on transplanted adipose-derived stem cells in vivo is largely unknown. Methods: This study focused on exploring the effects of plasma HDL on ADSC and delineating the mechanisms involved in their proliferation after entering the bloodstream. Using the MTT and BrdU assays, we tested the effects of HDL on ADSC proliferation. We probed the downstream intracellular Akt and ERK1/2 signaling pathways and expression of cyclin proteins in ADSC using western blot. Results: Our study found that HDL promotes proliferation of ADSC, by binding to sphingosine-1-phosphate receptor-1(S1P1) on the cell membrane. This interaction led to activation of intracellular Akt and ERK1/2 signaling pathways, resulting in increased expression of cyclin D1 and cyclin E, and simultaneous reduction in expression of cyclin-dependent kinase inhibitors p21 and p27, therefore promoting cell cycle progression and cell proliferation. Conclusions: These studies raise the possibility that HDL may be a physiologic regulator of stem cells and increasing HDL concentrations may be valuable strategy to promote ADSC transplantation.'973' National ST Major Project [2011CB503900]; National Natural Science Foundation of China [81270321, 81170101, 81370235]; Natural Science Foundation of Beijing, China [7122106]SCI(E)[email protected]; [email protected]

Effects of iron oxides on the anaerobic codigestion performances of the Pennisetum hybrid and kitchen waste

The addition of iron oxides in anaerobic digestion can increase conversion efficiency. In this study, we investigated the effects of the addition of Fe2O3, Fe2O3 nanoparticles, Fe3O4, and Fe3O4 nanoparticles with different concentrations (0.5%–1.5%) on the anaerobic codigestion of a Pennisetum hybrid and kitchen waste in a batch-mode mesophilic experiment. The results indicated that the additives with different valence states and particle sizes had different effects on the anaerobic codigestion of the Pennisetum hybrid and kitchen waste. The addition of 0.5% Fe2O3 [with a biogas production of 286.0±61.8  mL/g volatile solid (VS)] and 0.5% Fe3O4 (with a biogas production of 309.1±22.3  mL/g VS) improved the cumulative biogas yield by 23.5% and 37.9%, respectively, compared with that of the control group (with a biogas production of 237.2±30.1  mL/g VS). Further correlation analysis showed that pH and total ammonia nitrogen were positively correlated with cumulative biogas yield, whereas bicarbonate alkalinity concentration/volatile alkalinity concentration and volatile fatty acids were negatively correlated with cumulative biogas yield. This study provided insights on anaerobic codigestion of the Pennisetum hybrid and kitchen waste in the presence of iron oxides, which will be beneficial for further studies in the field of renewable energy production

Microscopic description of nuclei in the middle of the pf-shell by a shell model calculation with G-matrix interaction

Energy levels and electromagnetic properties of with $N=28\sim 30$ nuclides are studied in terms of a large-scale shell model calculation, which contains no newly adjusted parameters. The Kuo-Brown $G$-matrix interaction is shown to reproduce energy levels of 205 low-lying states of these nuclei. We evaluate effective charges by incorporating the core-polarization effects caused by the coupling to GQR's. We then compute E2 moments and transition probabilities. The M1 moments and transition rates are calculated by quoting the effective $g$-factors of Towner, which are obtained by taking into account the meson-exchange and the core-polarization mechanisms. By this microscopic calculation most of the E2 properties and the magnetic moments are reproduced. Although there are agreements and disagreements in the M1 transition rates, the general tendency is reproduced. The $(e,e')$ and $(p,p')$ excitation from the ground state to some low-lying $2^+$ states is also discussed.Comment: 63 pages (LaTeX, to be published in Nucl. Phys. A

Colesevelam enhances the beneficial effects of brown fat activation on hyperlipidemia and atherosclerosis development

Aims Brown fat activation accelerates the uptake of cholesterol-enriched remnants by the liver and thereby lowers plasma cholesterol, consequently protecting against atherosclerosis development. Hepatic cholesterol is then converted into bile acids (BAs) that are secreted into the intestine and largely maintained within the enterohepatic circulation. We now aimed to evaluate the effects of prolonged brown fat activation combined with inhibition of intestinal BA reabsorption on plasma cholesterol metabolism and atherosclerosis development and results APOE∗3-Leiden.CETP mice with humanized lipoprotein metabolism were treated for 9 weeks with the selective b3-adrenergic receptor (AR) agonist CL316,243 to substantially activate brown fat. Prolonged b3-AR agonism reduced faecal BA excretion (-31%), while markedly increasing plasma levels of total BAs (258%), cholic acid-derived BAs (295%), and chenodeoxycholic acid-derived BAs (217%), and decreasing the expression of hepatic genes involved in BA production. In subsequent experiments, mice were additionally treated with the BA sequestrant Colesevelam to inhibit BA reabsorption. Concomitant intestinal BA sequestration increased faecal BA excretion, normalized plasma BA levels, and reduced hepatic cholesterol. Moreover, concomitant BA sequestration further reduced plasma total cholesterol (-49%) and non-high-density lipoprotein cholesterol (-56%), tended to further attenuate atherosclerotic lesion area (-54%). Concomitant BA sequestration further increased the proportion of lesion-free valves (34%) and decreased the relative macrophage area within the lesion (-26%), thereby further increasing the plaque stability index (44%). Conclusion BA sequestration prevents the marked accumulation of plasma BAs as induced by prolonged brown fat activation, thereby further improving cholesterol metabolism and reducing atherosclerosis development. These data suggest that combining brown fat activation with BA sequestration is a promising new therapeutic strategy to reduce hyperlipidaemia and cardiovascular diseases

Inhibition of DHCR24 activates LXRα to ameliorate hepatic steatosis and inflammation

Liver X receptor (LXR) agonism has theoretical potential for treating NAFLD/NASH, but synthetic agonists induce hyperlipidemia in preclinical models. Desmosterol, which is converted by Δ24-dehydrocholesterol reductase (DHCR24) into cholesterol, is a potent endogenous LXR agonist with anti-inflammatory properties. We aimed to investigate the effects of DHCR24 inhibition on NAFLD/NASH development. Here, by using APOE*3-Leiden. CETP mice, a well-established translational model that develops diet-induced human-like NAFLD/NASH characteristics, we report that SH42, a published DHCR24 inhibitor, markedly increases desmosterol levels in liver and plasma, reduces hepatic lipid content and the steatosis score, and decreases plasma fatty acid and cholesteryl ester concentrations. Flow cytometry showed that SH42 decreases liver inflammation by preventing Kupffer cell activation and monocyte infiltration. LXRα deficiency completely abolishes these beneficial effects of SH42. Together, the inhibition of DHCR24 by SH42 prevents diet-induced hepatic steatosis and inflammation in a strictly LXRα-dependent manner without causing hyperlipidemia. Finally, we also showed that SH42 treatment decreased liver collagen content and plasma alanine transaminase levels in an established NAFLD model. In conclusion, we anticipate that pharmacological DHCR24 inhibition may represent a novel therapeutic strategy for treatment of NAFLD/NASH.</p

Deletion of hematopoietic Dectin-2 or CARD9 does not protect against atherosclerotic plaque formation in hyperlipidemic mice

Inflammatory reactions activated by pattern recognition receptors (PRRs) on the membrane of innate immune cells play an important role in atherosclerosis. Whether the PRRs of the C-type lectin receptor (CLR) family including Dectin-2 may be involved in the pathogenesis of atherosclerosis remains largely unknown. Recently, the CLR-adaptor molecule caspase recruitment domain family member 9 (CARD9) has been suggested to play a role in cardiovascular pathologies as it provides the link between CLR activation and transcription of inflammatory cytokines as well as immune cell recruitment. We therefore evaluated whether hematopoietic deletion of Dectin-2 or CARD9 reduces inflammation and atherosclerosis development. Low-density lipoprotein receptor (Ldlr)- knockout mice were transplanted with bone marrow from wild-type, Dectin-2- or Card9-knockout mice and fed a Western-type diet containing 0.1% (w/w) cholesterol. After 10 weeks, lipid and inflammatory parameters were measured and atherosclerosis development was determined. Deletion of hematopoietic Dectin-2 or CARD9 did not influence plasma triglyceride and cholesterol levels. Deletion of hematopoietic Dectin-2 did not affect atherosclerotic lesion area, immune cell composition, ex vivo cytokine secretion by peritoneal cells or bone marrow derived macrophages. Unexpectedly, deletion of hematopoietic CARD9 increased atherosclerotic lesion formation and lesion severity. Deletion of hematopoietic CARD9 did also not influence circulating immune cell composition and peripheral cytokine secretion. Besides a tendency to a reduced macrophage content within these lesions, plasma MCP-1 levels decreased upon WTD feeding. Deletion of hematopoietic Dectin-2 did not influence atherosclerosis development in hyperlipidemic mice. The absence of CARD9 unexpectedly increased atherosclerotic lesion size and severity, suggesting that the presence of CARD9 may protect against initiation of atherosclerosis development