Chemo-Sensitive Running Droplet

Chemical control of the spontaneous motion of a reactive oil droplet moving on a glass substrate under an aqueous phase is reported. Experimental results show that the self-motion of an oil droplet is confined on an acid-treated glass surface. The transient behavior of oil-droplet motion is also observed with a high-speed video camera. A mathematical model that incorporates the effect of the glass surface charge is built based on the experimental observation of oil-droplet motion. A numerical simulation of this mathematical model reproduced the essential features concerning confinement within a certain chemical territory of oil-droplet motion, and also its transient behavior. Our results may shed light on physical aspects of reactive spreading and a chemotaxis in living things.Comment: 17 pages, 10 figure

Gene Expression Profiles of the Cochlea and Vestibular Endorgans: Localization and Function of Genes Causing Deafness

Objectives: We sought to elucidate the gene expression profiles of the causative genes as well as the localization of the encoded proteins involved in hereditary hearing loss. Methods: Relevant articles (as of September 2014) were searched in PubMed databases, and the gene symbols of the genes reported to be associated with deafness were located on the Hereditary Hearing Loss Honnepage using localization, expression, and distribution as keywords. Results: Our review of the literature allowed us to systematize the gene expression profiles for genetic deafness in the inner ear, clarifying the unique functions and specific expression patterns of these genes in the cochlea and vestibular endorgans. Conclusions: The coordinated actions of various encoded molecules are essential for the normal development and maintenance of auditory and vestibular function.ArticleANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY. 124:6S-48S (2015)journal articl

Studies of Multiple Endocrine Neoplasia Type 2A Syndrome: Linkage Analyses and Comparison of Constitutional and Tumor Genotypes

Linkage analyses were carried out in nine Japanese kindreds with multiple endocrine neoplasia type 2A (MEN-2A) using polymorphic classical markers and DNA markers. We excluded close linkage of the MEN-2A gene (MEN2A) locus with Gm, JK, PGMl, and a DNA segment, D20S5, which is assigned to band 12 of the short arm of chromosome 20 (20p12.2). Assuming that MEN2A is recessive at the cellular level as in retinoblastoma (RB) and Wilms\u27 tumor (WT). comparison of constitutional and tumor genotypes may be useful in the search for the MEN2A locus. When DNA samples from 12 patients with medullary thyroid carcinoma (MTC) were compared with 15 polymorphic DNA markers including two assigned to chromosome 20, the results were negative. Both the negative linkage data and the failure to find loss of heterozygosity in MTC with chromosome 20 probes suggest that MEN2A may not be at 20p12.2, which was previously suggested as the site of an inherited chromosomal deletion in MEN-2A

An Open-labeled, Multicenter Phase II Study of Tamibarotene in Patients with Steroid-refractory Chronic Graft-versus-Host Disease

Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity following allogeneic hematopoietic cell transplantation (HSCT). Retinoic acid (tamibarotene) exerts multiple effects on cell differentiation and is clinically used for the treatment of acute promyelocytic leukemia. Tamibarotene down-regulates both Th1 and Th17 differentiation in donor T cells after allogeneic HSCT, resulting in attenuation of experimental chronic GVHD. Based on preclinical data, we have launched a phase II study of tamibarotene in patients with steroid-refractory chronic GVHD. This study will clarify whether tamibarotene can exert beneficial effects in patients with steroid-refractory chronic GVHD

Renormalization-group Method for Reduction of Evolution Equations; invariant manifolds and envelopes

The renormalization group (RG) method as a powerful tool for reduction of evolution equations is formulated in terms of the notion of invariant manifolds. We start with derivation of an exact RG equation which is analogous to the Wilsonian RG equations in statistical physics and quantum field theory. It is clarified that the perturbative RG method constructs invariant manifolds successively as the initial value of evolution equations, thereby the meaning to set $t_0=t$ is naturally understood where $t_0$ is the arbitrary initial time. We show that the integral constants in the unperturbative solution constitutes natural coordinates of the invariant manifold when the linear operator $A$ in the evolution equation has no Jordan cell; when $A$ has a Jordan cell, a slight modification is necessary because the dimension of the invariant manifold is increased by the perturbation. The RG equation determines the slow motion of the would-be integral constants in the unperturbative solution on the invariant manifold. We present the mechanical procedure to construct the perturbative solutions hence the initial values with which the RG equation gives meaningful results. The underlying structure of the reduction by the RG method as formulated in the present work turns out to completely fit to the universal one elucidated by Kuramoto some years ago. We indicate that the reduction procedure of evolution equations has a good correspondence with the renormalization procedure in quantum field theory; the counter part of the universal structure of reduction elucidated by Kuramoto may be the Polchinski's theorem for renormalizable field theories. We apply the method to interface dynamics such as kink-anti-kink and soliton-soliton interactions in the latter of which a linear operator having a Jordan-cell structure appears.Comment: 67 pages. No figures. v2: Additional discussions on the unstable motion in the the double-well potential are given in the text and the appendix added. Some references are also added. Introduction is somewhat reshape

Peripheral Blood as a Preferable Source of Stem Cells for Salvage Transplantation in Patients with Graft Failure after Cord Blood Transplantation: A Retrospective Analysis of the Registry Data of the Japanese Society for Hematopoietic Cell Transplantation

To compare the different stem cell sources used in salvage transplantation for graft failure (GF) after cord blood transplantation (CBT), we retrospectively analyzed data of 220 patients who developed GF after undergoing CBT between January 2001 and December 2007 and underwent a second hematopoietic stem cell transplantation (HSCT) within 3 months. The donor sources for salvage HSCT were cord blood (n = 180), peripheral blood stem cells (PBSCs; n = 24), and bone marrow (BM; n = 16). The cumulative incidence of neutrophil engraftment on day 30 after the second HSCT was 39% with CB, 71% with PBSCs, and 75% with BM. Multivariate analysis revealed that PBSC and BM grafts were associated with a significantly higher engraftment rate than CB (hazard ratio [HR], 7.77; P < .001 and HR, 2.81; P = .016, respectively). Although the incidence of grade II-IV acute graft-versus-host disease was significantly higher in the PBSC group than in the CB group (HR, 2.83; P = .011), the incidence of 1-year nonrelapse mortality was lower in the PBSC group than in the CB group (HR, 0.43; P = .019), and 1-year overall survival was superior in the PBSC group compared with the CB group (HR, 0.45; P = .036). Our results suggest that PBSC is the preferable source of stem cells in salvage HSCT for GF after CBT

腸管出血性大腸菌経口感染マウスに誘導される腸管内特異免疫応答

腸管粘膜感染菌である腸管出血性大腸菌(enterohemorrhagic Escherichia coli、EHEC)O157:H7の経口感染マウスを用い、粘膜免疫応答の誘導機構の解析を行った。特異抗体は、EHEC O157:H7菌体(Whole cell)を抗原とした酵素免疫測定法(Filtration ELISA)を用い、菌体表面に対する抗体価として評価した。EHEC野生株をICRマウスに経胃接種した場合、本菌は盲腸上皮細胞に接着して4週間以上定着し、接種4週後の糞便中にEHEC菌体に対するIgA抗体の著明な上昇がみられた。一方、EHECの上皮細胞への接着に関わる因子の遺伝子を変異させた菌株はマウス腸管への定着性を示さず、糞便中IgA抗体の誘導もみられなかった。変異株は繰り返し接種しても血中抗体は誘導されるものの糞便中IgA抗体は誘導されなかった。さらに、マウスを抗生物質処置することによって変異株を腸管内に長期定着させた場合も、糞便中IgA抗体は誘導されなかった。以上のように、EHECの上皮細胞への接着は全身性免疫応答の誘導には必ずしも必要ではないが、粘膜免疫応答の誘導には必須であることが示された。The induction mechanism of mucosal immune responses was examined in mice infected orally with an intestinal pathogen, enterohemorrhagic Escherichia coli (EHEC) O157:H7. Antibodies were evaluated as those specific to EHEC O157:H7 cell surface by enzyme linked-immunosorbent assay using EHEC O157:H7 whole cells as an antigen (Filtration ELISA). When the EHEC wild type was inoculated intragastlically into ICR mice, the bacteria adhered on the cecal epithelia and colonized over four weeks, and fecal IgA antibody to the EHEC whole cells markedly increased at four weeks after the inoculation. On the other hand, mutants deleted adherent factors of the EHEC did not colonize in the intestine and did not induce fecal IgA antibody. When the mutant was inoculated repeatedly, fecal IgA antibody was not induced although the serum antibodies were induced. Furthermore, the fecal IgA antibody was not induced even when the mutants resided persistently in the intestine of mice by treatment with an antibiotic. Thus, the adhesion of EHEC to epithelial cells was indispensable to induce the mucosal immune responses but not systemic immune responses