An a posteriori verification method for generalized real-symmetric eigenvalue problems in large-scale electronic state calculations

An a posteriori verification method is proposed for the generalized real-symmetric eigenvalue problem and is applied to densely clustered eigenvalue problems in large-scale electronic state calculations. The proposed method is realized by a two-stage process in which the approximate solution is computed by existing numerical libraries and is then verified in a moderate computational time. The procedure returns intervals containing one exact eigenvalue in each interval. Test calculations were carried out for organic device materials, and the verification method confirms that all exact eigenvalues are well separated in the obtained intervals. This verification method will be integrated into EigenKernel (https://github.com/eigenkernel/), which is middleware for various parallel solvers for the generalized eigenvalue problem. Such an a posteriori verification method will be important in future computational science.Comment: 15 pages, 7 figure

Cl-35 NQR study of lattice dynamic and magnetic property of a crystalline coordination polymer {CuCA(phz)(H2O)2}n

Copper(II) compounds {CuCA(phz)(H2O)2}n (H2CA = chloranilic acid, phz = phenazine) having a layer structure of -CuCA(H2O)2- polymer chains and phenazine was studied by 35Cl nuclear quadrupole resonance (NQR). The single NQR line observed at 35.635 MHz at 261.5 K increased to 35.918 MHz at 4.2 K. The degree of reduction of electric field gradient due to lattice vibrations was similar to that of chloranilic acid crystal. Temperature dependence of spin-lattice relaxation time, T1, of the 35Cl NQR signal below 20 K, between 20 and 210 K, and above 210 K, was explained by 1) a decrease of effective electron-spin density caused by antiferromagnetic interaction, 2) a magnetic interaction between Cl nuclear-spin and electron-spins on paramagnetic Cu(II) ions, and 3) an increasing contribution from reorientation of ligand molecules, respectively. The electron spin-exchange parameter |J| between the neighboring Cu(II) electrons was estimated to be 0.33 cm−1 from the T1 value of the range 20−210 K. Comparing this value with that of J = −1.84 cm−1 estimated from the magnetic susceptibility, it is suggested that the magnetic dipolar 2 coupling with the electron spins on Cu(II) ions must be the principal mechanism for the 35Cl NQR spin-lattice relaxation of {CuCA(phz)(H2O)2}n but a delocalization of electron spin over the chloranilate ligand have to be taken into account.</p

Chocolate as a food matrix reduces the bioavailability of galloylated catechins from green tea in healthy women

In this study, we evaluated the food matrix effects of chocolate on absorption of green tea catechins (GTCs), (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECg), and (−)-epigallocatechin gallate (EGCg), in five healthy 22-year-old women. In the single-intake experiment, the plasma concentrations of ECg (P < 0.05, at 1.5 h) and EGCg (P < 0.05, at 6 h) but not those of EC and EGC were reduced by the chocolate matrix. Regardless of the chocolate matrix, ECg and EGCg were mainly present as their aglycones in the plasma, whereas EGC and EC were found mostly as conjugated metabolites. After daily intake of GTCs mixed with chocolate for 14 days followed by overnight fasting, ECg but not EGCg was detected in the plasma. To compare the plasma profiles of ECg and EGCg, a mixture containing approximately equal amounts of ECg and EGCg was administered to nine rats for 14 days. Following treatment and overnight food deprivation, the plasma content of ECg was higher than that of EGCg. After a single injection of the same mixture in seven rats, ECg levels were higher than those of EGCg, and a greater amount of conjugated metabolites of ECg than those of EGCg was detected in the plasma 10 h after administration. In conclusion, the chocolate matrix affects the plasma profiles of GTCs, particularly ECg. ECg appears to persist in the plasma for a longer period, regardless of the chocolate matrix

Ion irradiation of multi-walled boron nitride nanotubes

Non Peer reviewe

Prevention of Disuse Muscle Atrophy by Dietary Ingestion of 8-Prenylnaringenin in Denervated Mice

Flavonoids have attracted considerable attention in relation to their effects upon health. 8-Prenylnaringenin (8-PN) is found in the common hop (Humulus lupulus) and assumed to be responsible for the health impact of beer consumption. We wanted to clarify the effects of prenylation on the physiological functions of dietary flavonoids by comparing the effects of 8-PN with that of intact naringenin in the prevention of disuse muscle atrophy using a model of denervation in mice. Consumption of 8-PN (but not naringenin) prevented loss of weight in the gastrocnemius muscle further supported by the lack of induction of the protein content of a key ubiquitin ligase involved in muscle atrophy, atrogin-1, and by the activation of Akt phosphorylation. 8-PN content in the gastrocnemius muscle was tenfold higher than that of naringenin. These results suggested that, compared with naringenin, 8-PN was effectively concentrated into skeletal muscle to exert its preventive effects upon disuse muscle atrophy. It is likely that prenylation generates novel functions for 8-PN by enhancing its accumulation into muscle tissue through dietary intake

DNA Methylation Profiles of the Brain-Derived Neurotrophic Factor (BDNF) Gene as a Potent Diagnostic Biomarker in Major Depression

Major depression, because of its recurring and life-threatening nature, is one of the top 10 diseases for global disease burden. Major depression is still diagnosed on the basis of clinical symptoms in patients. The search for specific biological markers is of great importance to advance the method of diagnosis for depression. We examined the methylation profile of 2 CpG islands (I and IV) at the promoters of the brain-derived neurotrophic factor (BDNF) gene, which is well known to be involved in the pathophysiology of depression. We analyzed genomic DNA from peripheral blood of 20 Japanese patients with major depression and 18 healthy controls to identify an appropriate epigenetic biomarker to aid in the establishment of an objective system for the diagnosis of depression. Methylation rates at each CpG unit was measured using a MassArray (R) system (SEQUENOM), and 2-dimensional hierarchical clustering analyses were undertaken to determine the validity of these methylation profiles as a diagnostic biomarker. Analyses of the dendrogram from methylation profiles of CpG I, but not IV, demonstrated that classification of healthy controls and patients at the first branch completely matched the clinical diagnosis. Despite the small number of subjects, our results indicate that classification based on the DNA methylation profiles of CpG I of the BDNF gene may be a valuable diagnostic biomarker for major depression

8-PN promotes recovery from muscle atrophy via Akt pathway

8-Prenylnaringenin (8-PN) is a prenylflavonoid that originates from hop extracts and is thought to help prevent disuse muscle atrophy. We hypothesized that 8-PN affects muscle plasticity by promoting muscle recovery under disuse muscle atrophy. To test the promoting effect of 8-PN on muscle recovery, we administered an 8-PN mixed diet to mice that had been immobilized with a cast to one leg for 14 days. Intake of the 8-PN mixed diet accelerated recovery from muscle atrophy, and prevented reductions in Akt phosphorylation. Studies on cell cultures of mouse myotubes in vitro demonstrated that 8-PN activated the PI3K/Akt/P70S6K1 pathway at physiologic concentrations. A cell-culture study using an inhibitor of estrogen receptors and an in vivo experiment with ovariectomized mice suggested that the estrogenic activity of 8-PN contributed to recovery from disuse muscle atrophy through activation of an Akt phosphorylation pathway. These data strongly suggest that 8-PN is a naturally occurring compound that could be used as a nutritional supplement to aid recovery from disuse muscle atrophy

ヒトマクロファージ様細胞株U937細胞におけるアセチルコリン受容体の生理的役割の検討

白血球の一種マクロファージ（Mφ）は、自然免疫と獲得免疫の両方に関与する免疫細胞である。さらに、Mφは、種々の生理活性物質を産生し、多くの炎症性疾患を始めとする様々な疾患の病態形成に深く関わっている。Mφには、ムスカリン性およびニコチン性アセチルコリン受容体 (mAChRおよびnAChR) が発現している。Mφ上のα7型 nAChRは、炎症性サイトカイン腫瘍壊死因子-αの遊離抑制や抗原提示機能の調節に関与していることが報告されている。本研究では、MφにおけるAChRの役割を明らかにしていく目的で、Mφの活性化がAChRの遺伝子発現に及ぼす影響を検討した。さらに、Mφの炎症性遺伝子発現制御機構におけるAChRの生理的役割を検討した。ヒトマクロファージ様細胞株U937細胞をMφモデルとして使用した。U937細胞において、LPSによる活性化は、M1、M3、M5サブタイプmAChR mRNA、およびα4、β2 サブユニットnAChR mRNAの発現を増大させた。U937細胞において、LPSは、COX-2 mRNAの発現を増大させた。しかしながら、mAChRあるいはnAChRの活性化だけでは、COX-2 mRNA発現は影響を受けなかった。nAChRの活性化は、LPSによるCOX-2 mRNA発現の増大を抑制したが、mAChRの活性化はLPSによるCOX-2 mRNA発現の増大には影響しなかった。以上の結果より、Mφの活性化によりmAChRおよびnAChRの発現が増大することが明らかとなった。さらに、U937細胞におけるCOX-2の発現制御機構において、TLR4を介したMφの活性化によるCOX-2 mRNAの発現増大は、nAChRを介した機構によって抑制されることが示唆された。A type of white blood cells, macrophage (Mφ) is an immune cell involved in both innate and acquired immunity. Furthermore, Mφ produces various physiologically active substances and is deeply involvedin the pathogenesis of various diseases including many inflammatory diseases. Mφs express muscarinic and nicotinic acetylcholine receptors (mAChR and nAChR). It has been reported that α7 type nAChR on Mφ is involved in reducing the release of pro-inflammatory cytokine tumor necrosis factor-α and regulating antigen presentation function. In this study, we investigated the effect of Mφ activation on AChR gene expression in order to clarify the role of AChR in Mφ. Furthermore, we investigated the physiological role of AChR in the regulation mechanism of inflammatory gene expression of Mφ. Human macrophage-like cell line U937 cells were used as an Mφ model. In U937 cells, the presence of LPS increased the expression of M1, M3, M5 subtype mAChR mRNA, and α4, β2 subunit nAChR. In U937 cells, LPS increased COX-2 mRNA expression. However, activation of mAChR or nAChR alone did not affect COX-2 mRNA expression. nAChR activation suppressed the increase in COX-2 mRNA expression by LPS, whereas mAChR activation did not affect the increase in COX-2 mRNA expression by LPS. From the above results, it was clarified that the expression of mAChR and nAChR increases by Mφ activation. Furthermore, in the COX-2 expression control mechanism in U937 cells, it was suggested that the increase in COX-2 expression due to Mφ activation via TLR4 is suppressed by the mechanism via nAChR.論