Purification, identification and phosphorylation of annexin I from rat liver mitochondria.

Annexin was purified from rat liver mitochondria to an apparent homogeneity with a molecular weight of 35 kDa as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The purified mitochondrial annexin (AXmito) was identified as annexin I by an immunoblot analysis using anti-annexin I antibody. The inhibitory effect of AXmito I on porcine pancreatic phospholipase A2 activity was as potent as that of bovine lung annexin I. The presence of annexin I in mitochondria was confirmed by an electron-microscopic study. AXmito I was shown to be phosphorylated by intrinsic protein tyrosine kinases on its tyrosine residues. This annexin was also phosphorylated by protein kinase C.</p

Crystallization and preliminary X-ray structural studies of human prouroguanylin. Corrigendum

A corrigendum to the article by Ito et al. [Acta Cryst. (2008). F64, 531–532]

Derivation of the Konishi anomaly relation from Dijkgraaf-Vafa with (Bi-)fundamental matters

We explicitly write down the Feynman rules following the work of Dijkfraaf, Vafa and collaborators for N=1 super Yang-Mills having products of SU groups as the gauge group and matter chiral superfields in adjoint, fundamental, and bi-fundamental representations without baryonic perturbations. As an application of this, we show expectation values calculated by these methods satisfy the Konishi anomaly relation.Comment: 6 pages, no figures. v2: A few arguments improved, conclusion not change

Soluble Klotho causes hypomineralization in Klotho-deficient mice

The type I transmembrane protein αKlotho (Klotho) serves as a coreceptor for the phosphaturic hormone fibroblast growth factor 23 (FGF23) in kidney, while a truncated form of Klotho (soluble Klotho, sKL) is thought to exhibit multiple activities, including acting as a hormone, but whose mode(s) of action in different organ systems remains to be fully elucidated. FGF23 is expressed primarily in osteoblasts/osteocytes and aberrantly high levels in the circulation acting via signaling through an FGF receptor (FGFR)-Klotho coreceptor complex cause renal phosphate wasting and osteomalacia. We assessed the effects of exogenously added sKL on osteoblasts and bone using Klotho-deficient (kl/kl) mice and cell and organ cultures. sKL induced FGF23 signaling in bone and exacerbated the hypomineralization without exacerbating the hyperphosphatemia, hypercalcemia and hypervitaminosis D in kl/kl mice. The same effects were seen in rodent bone models in vitro, in which we also detected formation of a sKL complex with FGF23-FGFR and decreased Phex (gene responsible for X-linked hypophosphatemic rickets (XLH)/osteomalacia) expression. Further, sKL-FGF23-dependent hypomineralization in vitro was rescued by soluble PHEX. These data suggest that exogenously added sKL directly participates in FGF23 signaling in bone and that PHEX is a downstream effector of the sKL-FGF23-FGFR axis in bone.This work was supported in part by grants from the Ministry of Education, Science, Sports and Culture, Japan (18592001 and 20592139 to Y Y and 21791788 to T M), and the Canadian Institutes of Health Research (MOP 83704 to J E A)

Structure Effect on Antioxidant Activity of Catecholamines toward Singlet Oxygen and Other Reactive Oxygen Species in vitro

The reactivity of catecholamine neurotransmitters and the related metabolites were precisely investigated toward 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and reactive oxygen species. Catecholamines reacted immediately with DPPH radicals, their reactivity being stronger than that of ascorbic acid as a reference. Superoxide scavenging activities of catecholamines determined by WST-1 and electron spin resonance (ESR) spin trapping methods were also high. Whereas tyrosine, the dopamine precursor showed no reactivity toward superoxide. The reactivity toward singlet oxygen was evaluated by observing specific photon emission from singlet oxygen. The results revealed that reactivity of catecholamines was markedly higher than that of sodium azide, and catechin as catechol reference. The reaction of catecholamines and singlet oxygen was further studied by ESR using 55-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trapping reagent and rose bengal as photosensitizer. DMPO-OH signal of epinephrine was significantly small compared to other catecholamines, catechin, and 4-methylcatechol as a reference compound and was as small as that of tyrosine. The signal formation was totally dependent on singlet oxygen, and the presence of catechol compounds. These results indicated that epinephrine is the most potent singlet oxygen quencher than other catecholamines, and the secondary amino group in its alkyl side chain could play a role in unique singlet oxygen quenching property of epinephrine

CFT Description of String Theory Compactified on Non-compact Manifolds with G_2 Holonomy

We construct modular invariant partition functions for strings propagating on non-compact manifolds of G_2 holonomy. Our amplitudes involve a pair of N=1 minimal models M_m, M_{m+2} (m=3,4,...) and are identified as describing strings on manifolds of G_2 holonomy associated with A_{m-2} type singularity. It turns out that due to theta function identities our amplitudes may be cast into a form which contain tricritical Ising model for any m. This is in accord with the results of Shatashvili and Vafa. We also construct a candidate partition function for string compactified on a non-compact Spin(7) manifold.Comment: It is found that tricritical Ising model is contained in our amplitues in agreement with the results of Shatashvili and Vafa. Manuscript is revised accordingly. A new reference is also adde

The usefulness of nifekalant for activation mapping of premature beat-triggered atrial fibrillation: Suppression of atrial fibrillation initiation without inhibiting premature beat

AbstractA 66-year-old man underwent a second ablation for atrial fibrillation (AF). Intravenous isoproterenol administration caused the atrial premature beat (APB), triggering AF. The APB originated in the right atrium and invariably initiated AF. Therefore, contact activation mapping could not be performed without frequent electrocardioversion. To prevent the initiation of AF without inhibiting the APB firing, we administered nifekalant intravenously, which facilitated precise activation mapping and ablation of the AF-triggering APB. The administration of nifekalant may improve clinical outcomes of catheter ablation for AF triggered by non-pulmonary vein APB, which invariably initiates AF