Thick Domain Walls Intersecting a Black Hole

We discuss the gravitationally interacting system of a thick domain wall and a black hole. We numerically solve the scalar field equation in the Schwarzschild spacetime and show that there exist scalar field configurations representing thick domain walls intersecting the black hole.Comment: 14 pages, 8 figure

A single Gly114Arg mutation stabilizes the hexameric subunit assembly and changes the substrate specificity of halo-archaeal nucleoside diphosphate kinase

AbstractNucleoside diphosphate kinase from extremely halophilic archaeon (HsNDK) requires above 2M NaCl concentration for in vitro refolding. Here an attempt was made to isolate mutations that allow HsNDK to refold in low salt media. Such a screening resulted in isolation of an HsNDK mutant, Gly114Arg, which efficiently refolded in the presence of 1M NaCl. This mutant, unlike the wild type enzyme, was expressed in Escherichia coli as an active form. The residue 114 is in close proximity to Glu155 of the neighboring subunit in the three dimensional hexameric structure of the HsNDK. It is thus possible that the attractive electrostatic interactions occur between Arg114 and Glu155 in the mutant HsNDK, stabilizing the hexameric subunit assembly

Enlargement of accessory spleen subsequent to splenectomy associated with gastrectomy can mimic a solitary tumor : report of a case

We report a case of a 65-year-old woman with an incidental about 20-mm solitary mass between the lateralsegment of the left lobe of the liver and left kidney 5 years after splenectomy associated with total gastrectomy. The mass wassurgically resected, and histological examination revealed it to be an accessory spleen. Small accessory spleens mostly locatednear the splenic hilus, but large accessory spleens are unusual after total gastrectomy with regional lymph nodes resection. Theremaining accessory splenic tissue would undergo compensatory hypertrophy. Hence, the possibility of accessory spleens mustbe considered when an intra-abdominal mass is identified in a patient with splenectomy associated with gastrectomy

Immunomodulating Activity of Agaricus brasiliensis KA21 in Mice and in Human Volunteers

We performed studies on murine models and human volunteers to examine the immunoenhancing effects of the naturally outdoor-cultivated fruit body of Agaricus brasiliensis KA21 (i.e. Agaricus blazei). Antitumor, leukocyte-enhancing, hepatopathy-alleviating and endotoxin shock-alleviating effects were found in mice. In the human study, percentage body fat, percentage visceral fat, blood cholesterol level and blood glucose level were decreased, and natural killer cell activity was increased. Taken together, the results strongly suggest that the A. brasiliensis fruit body is useful as a health-promoting food

Synthetic Study on [3,9-13C]-N-Acetylneuraminic Acid and Its Analogs

日本化学会第75秋季年会,平成10年9月15日,松山　講演番号：2 P1A0 63　化学関係学協会連合協議会研究発表

Synthetic Study on dl-Corchoionoside

講演番号：1 A1 14 日本化学会第76春季年会, 平成11年3月28日～3月31日, 横

RSV replication is attenuated by counteracting expression of the suppressor of cytokine signaling (SOCS) molecules

AbstractHuman RSV causes an annual epidemic of respiratory tract illness in infants and in elderly. Mechanisms by which RSV antagonizes IFN-mediated antiviral responses include inhibition of type I IFN mRNA transcription and blocking signal transduction of JAK/STAT family members. The suppressor of cytokines signaling (SOCS) gene family utilizes a feedback loop to inhibit cytokine responses and block the activation of the JAK/STAT signaling pathway. To evaluate the potential of SOCS molecules to subvert the innate immune response to RSV infection, eight SOCS family genes were examined. RSV infection up-regulated SOCS1, SOCS3, and CIS mRNA expression in HEp-2 cells. Suppression of SOCS1, SOCS3 and CIS by short interfering ribonucleic acid (siRNA) inhibited viral replication. Furthermore, inhibition of SOCS1, SOCS3, or CIS activated type I IFN signaling by inducing STAT1/2 phosphorylation. These results suggest that RSV infection escapes the innate antiviral response by inducing SOCS1, SOCS3 or CIS expression in epithelial cells