Derivation of Non-isotropic Phase Equations from a General Reaction-Diffusion Equation

A non-isotropic version of phase equations such as the Burgers equation, the K-dV-Burgers equation, the Kuramoto-Sivashinsky equation and the Benney equation in the three-dimensional space is systematically derived from a general reaction-diffusion system by means of the renormalization group method.Comment: 21pages,no figure

Syntheses of Technetium β-Diketone and 8-Quinolinol Complexes

開始ページ、終了ページ: 冊子体のページ付

Combined effect of regulatory polymorphisms on transcription of UGT1A1 as a cause of Gilbert syndrome

<p>Abstract</p> <p>Background</p> <p>Gilbert syndrome is caused by defects in bilirubin UDP-glucuronosyltransferase (UGT1A1). The most common variation believed to be involved is A(TA)7TAA. Although several polymorphisms have been found to link with A(TA)7TAA, the combined effect of regulatory polymorphisms in the development of Gilbert syndrome remains unclear.</p> <p>Methods</p> <p>In an analysis of 15 patients and 60 normal subjects, we detected 14 polymorphisms and nine haplotypes in the regulatory region. We classified the 4-kbp regulatory region of the patients into: the TATA box including A(TA)7TAA; a phenobarbital responsive enhancer module including c.-3275T>G; and a region including other ten linked polymorphisms. The effect on transcription of these polymorphisms was studied.</p> <p>Results</p> <p>All haplotypes with A(TA)7TAA had c.-3275T>G and additional polymorphisms. In an <it>in-vitro </it>expression study of the 4-kbp regulatory region, A(TA)7TAA alone did not significantly reduce transcription. In contrast, c.-3275T>G reduced transcription to 69% of that of wild type, and the linked polymorphisms reduced transcription to 88% of wild type. Transcription of the typical regulatory region of the patients was 56% of wild type. Co-expression of constitutive androstane receptor (CAR) increased the transcription of wild type by a factor of 4.3. Each polymorphism by itself did not reduce transcription to the level of the patients, however, even in the presence of CAR.</p> <p>Conclusions</p> <p>These results imply that co-operation of A(TA)7TAA, c.-3275T>G and the linked polymorphisms is necessary in causing Gilbert syndrome.</p

Lessons learned from the preclinical drug discovery of asoprisnil and ulipristal for non-surgical treatment of uterine leiomyomas

Introduction: Uterine leiomyoma is the most common benign tumor in women during the reproductive years. Menorrhagia is the common symptom and accounts for the most frequent indication for hysterectomy. Thus, development of a novel drug for non-surgical treatment of uterine leiomyoma is needed for the betterment of women\u27s health. Area covered: This review introduces a translational research initiated by use of the levonorgestrel-releasing intrauterine system (LNG-IUS) for contraceptive purposes. During follow-up, a patient informed that heavy menstrual bleeding caused by uterine myoma was strikingly reduced after the insertion of device. The patient\u27s unexpected comment led the authors to perform clinical trials of LNG-IUS for the management of menorrhagia in women with uterine myomas and striking reduction in menorrhagia was obtained by the use of LNG-IUS. MRI examination, however, revealed that the volume of myomas decreased in some, but increased in the other instances. This unexpected finding with MRI directed the authors to characterize the effects of progesterone (P4) and progesterone receptor modulators (PRMs) on uterineleiomyoma cell growth in vitro. Expert opinion: In consistence with the in vitro data obtained, randomized controlled clinical trials of PRMs in patients with uterine leiomyomas at several institutions have demonstrated that oral administration of PRMs (asoprisnil and ulipristal) for 3 months reduced leiomyoma volume, resulting in a significant improvement of the associated symptoms. However, a novel pattern of PRM-associated endometrial changes was recognized in the endometrial pathology, demonstrating unusual epithelial types not seen in the normal menstrual cycle of a premenstrual woman. Thus, follow-up studies to determine whether the novel endometrial changes remain, disappear or progress to something else are needed for the possible long-term use of PRMs for the treatment of uterine leiomyoma

Supplementary Material for: The in vivo Inhibition of Oral Biofilm Accumulation and Streptococcus mutans by Ceramic Water

<p>Combustion-synthesized titanium carbide ceramics uniformly disperse silver, producing silver ions and hydroxyl radicals in water. This generates antimicrobial activity against various bacteria. One such bacterium is <i>Streptococcus mutans</i>, a gram-positive anaerobic bacterium known as a major pathogen of dental caries. In this study, we analyzed the inhibition of oral biofilms and <i>S. mutans</i> by ceramic water in in vitro and human studies. <i>S. mutans</i> strains showed significantly lower antimicrobial and sucrose-dependent adhesion activity in the presence of ceramic powder compared with untreated culture medium. Confocal microscopy revealed that <i>S. mutans</i> biofilm structures with ceramic powder were thin and coarse. Twenty-seven volunteers (13 males, 14 females; 18-37 years old, mean 25.2 years) were enrolled for subsequent studies. After each meal, one group was asked to rinse with ceramic water while the other rinsed with untreated water for 1 week. After 1 week, the rinsing contents were switched between the groups and the same protocol was followed for an additional week. After rinsing with ceramic water, the average plaque score was 43.0 ± 3.7, which was significantly lower than the baseline value (74.1 ± 5.7, <i>p </i>< 0.001). However, no significant difference was observed when rinsing with untreated water. In addition, the total number of <i>S. mutans</i> in saliva was significantly reduced after rinsing with ceramic water compared with untreated water (<i>p </i>< 0.05). These results suggest that ceramic water possesses antimicrobial activity against <i>S. mutans</i> and inhibits biofilm formation. Rinsing with ceramic water can also inhibit dental plaque formation and <i>S. mutans</i> colonization in humans.</p

A novel function of B lymphocytes from normal mice to suppress autoimmunity in (NZB × NZW)F1 mice

In systemic autoimmune-prone (NZB × NZW)F1 (NZB/W F1) mice, B-cell abnormalities characterized by hypergammaglobulinaemia accompanying autoantibodies have been thought to be a main cause of the disease. To examine a possible regulatory role of B cells in the disease manifestations, we injected, intravenously (i.v.), normal or autoimmune B cells into non-irradiated NZB/W F1 mice. The injection of splenic B cells from major histocompatibility (MHC)-matched or allogeneic normal mice caused a marked decrease in serum immunoglobulin G (IgG) levels of autoantibodies, delayed the appearance of proteinuria and prolonged life span, whereas treatment with splenic B cells from NZB/W F1 or X-linked immunodeficient (Xid) mice failed to suppress the autoimmunity. Moreover, in vitro polyclonal antibody responses to lipopolysaccharide (LPS) of NZB/W F1-derived B cells from the treated mice were markedly reduced. Interestingly, the treatment of NZB/W F1 mice at 16, 18 and 20 or at 20, 22 and 24 weeks of age was more effective than that at 6, 8 and 10 weeks. The treatment also inhibited the development of surface IgG+ (sIgG+) B cells and splenomegaly, prominent in aged NZB/W F1 mice. In addition, when untreated NZB/W F1 responding B cells were precultured with normal B cells in vitro for 3 days, they also diminished the autoantibody production to subsequent LPS stimulation. Hence, the present results imply a novel function of normal B cells to ameliorate autoimmune disease in NZB/W F1 mice by correcting their B-cell abnormalities, and indicate that NZB/W F1 and Xid mice possess defects in this regulatory B-cell function