Search Results - (Author, Cooperation:Y. Miyazaki)

2018-02-03

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Geosciences

Computer Science

Medicine

Natural Sciences in General

Physics

Biochemistry, Microbiology

2014-02-28

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD40/immunology ; B-Lymphocytes/*immunology/*metabolism/secretion ; Encephalomyelitis, Autoimmune, Experimental/*immunology ; Female ; Humans ; Immunity/*immunology ; Interleukin-10/metabolism ; Interleukins/immunology/*metabolism/secretion ; Lymphocyte Activation ; Macrophages/cytology/immunology ; Male ; Mice ; Plasma Cells/immunology/metabolism ; Salmonella Infections/*immunology/microbiology ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/immunology

2018-01-12

American Society of Hematology (ASH)

0006-4971

1528-0020

Biology

Medicine

Lymphoid Neoplasia, Clinical Trials and Observations

2018-01-12

American Society of Hematology (ASH)

0006-4971

1528-0020

Biology

Medicine

Lymphoid Neoplasia, Clinical Trials and Observations

2018-01-12

American Society of Hematology (ASH)

0006-4971

1528-0020

Biology

Medicine

Lymphoid Neoplasia, Clinical Trials and Observations

2018-04-27

The American Society for Microbiology (ASM)

0066-4804

1098-6596

Biology

Medicine

1365-2133

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Summary A topical vitamin D3, ointment (tacalcitol) was prescribed for patients with long-histing pruriginous lesions (four with prurigo nodularis und seven with subacuLe prurigo, four of whom had atopic dermatitis). Seven of 11 cases had not responded to a topical steroid ointment and even to occlusive application of the ointment. Nine of 11 cases showed a significant clinical response to this new regimen within 4 weeks. Epidermal FceR1(+) dendritic cells were increased in number in prurigo nodularis and reduced to normal level after the therapy. Topical vitamin D3 ointment might be an alternative therapy ibr steroid-resistant prurigo.

Electronic Resource

1365-2222

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

The repeated application of glucocorticoids (GC) on the skin augmented the inflammatory response of both allergic and irritant contact dermatitis in our studies.In order to further clarify the mechanism of such an augmentation of contact hypersensitivity (CHS), we investigated the modulatory effects of cytokines in the epidermis after the administration of GC at challenged sites in CHS.Diflucortolone valerate was applied to BALB/c mice on alternate days for a total of nine times. On day 12, they were contact sensitized with dinitrofluorobenzene (DNFB). Next, on day 17, one day after the last application of GC, they were challenged with DNFB on the ear. The whole challenged ear lobes were removed after a hapten challenge and then were analysed by the RT-PCR method or underwent an immunohistochemical analysis. To clarify the modulatory effects of cytokines in vivo, DNFB sensitized mice pre-treated with GC were injected with rIL-10, IL-1 receptor antagonist (ra) and anti-IL-1α monoclonal antibody (mAb) and thereafter were challenged with DNFB.A RT-PCR analysis has demonstrated IL-10 mRNA to be detected in the challenged skin of non-GC-pretreated mice but not in that of GC-pre-treated mice after challenge. On the other hand, the expression of IL-1α mRNA in the challenged skin of mice pretreated with GC was more strongly detected that that in mice without GC-pretreatment. Furthermore, an immuno-histochemical analysis in the challenge showed the expression of IL-10 in the skin showed the expression of IL-10 in the challenged epidermis of the non-GC-pretreated mice but not in the GC-pretreated mice and IL-1α was also strongly expressed in the epidermis of the GC-pretreated mice. A subcutaneous injection of anti-IL-1α mAb or IL-1 ra inhibited the augmented CHS reaction in the GC-pretreated mice. A subcutaneous injection of rIL-10 also inhibited the augmentation of the CHS reaction in the GC-pretreated mice; however, no such inhibition was observed in the non-GC-pretreated mice.These results indicated that both an up-regulation of IL-1α production and the inhibition of the IL-10 production in the epidermis at the challenged skin sites in the GC-pretreated mice appear to play a critical role in the GC-induced augmentation of murine CHS.

Electronic Resource

1440-1681

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

1. In the present study, using the euglycaemic hyperinsulinaemic glucose clamp technique, we investigated the effects of hyperinsulinaemia on sodium-water metabolism and the pressor system in obesity, both of which have been reported to be closely associated with insulin resistance and/or hyperinsulinaemia.2. Sixteen obese young subjects and 24 non-obese young subjects who were all normotensives, participated in this study. The 2h euglycaemic hyperinsulinaemic glucose clamp was performed in a fasting state. The mean glucose infusion rate needed to maintain a fasting blood sugar level (FBS) during the last 30 min of the clamp was used as an indicator of insulin sensitivity (M-value). Before and after the clamp, the following parameters were measured: creatinine clearance (Ccr); urinary excretion of sodium (UNaV); fractional excretion of sodium (FENa); plasma renin activity (PRA); plasma aldosterone concentration (PAC) and plasma noradrenaline concentration (PNA).3. The M-value was significantly lower in obese subjects compared with non-obese subjects, although FBS and fasting immunoreactive insulin levels were similar in both groups. UNaV and FENa fell only in obese subjects during the clamp, while Ccr showed no significant change in either group. PNA and PRA increased significantly and PAC tended to increase in both groups.4. These results suggest that obese subjects have insulin resistance with respect to glucose metabolism, but that urinary sodium excretion and the pressor system remain insulin-sensitive; the sensitivity of the sodium retaining action to hyperinsulinaemia was actually higher in obese subjects than in non-obese subjects. Therefore, if compensatory endogenous hyperinsulinaemia was raised by insulin resistance, these two factors may lead to chronic sodium retention and pressor system stimulation and, in turn, to hypertension in obesity.

Electronic Resource

1440-1797

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background: We have previously shown that eradication of Helicobacter pylori increases acid secretion in H. pylori-associated enlarged fold gastritis. Aim: To investigate whether locally produced interleukin-1β is possibly involved in the inhibition of acid secretion in H. pylori gastritis. Methods: IL-1β release from the gastric body mucosa was determined by short-term culture of biopsy specimens in 13 patients with enlarged fold gastritis (all H. pylori-positive), five H. pylori-positive and 10 H. pylori-negative patients without enlarged folds. The acid-inhibitory effect of locally produced IL-1β was examined by []〉14C]-aminopyrine uptake assay using isolated rabbit gastric glands. Results: IL-1β release was significantly greater in patients with enlarged fold gastritis, significantly correlated with both basal and tetragastrin-stimulated acid outputs in the H. pylori-positive patients (r = −0.591 and r = −0.641, respectively; P 〈 0.01), and significantly decreased with concomitant increases in acid secretions after eradication of H. pylori. [14C]-aminopyrine uptake was inhibited by IL-1β in a dose-dependent manner. Conclusions: Increased production of IL-1β caused by H. pylori infection is possibly involved in the inhibition of acid secretion in enlarged fold gastritis.

Electronic Resource

0006-291X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Chemistry and Pharmacology

Physics

Electronic Resource

0006-291X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Chemistry and Pharmacology

Physics

Electronic Resource

0378-1119

Recombinant DNA ; S1 mapping ; gene organization ; primer extension ; promoter analysis ; pseudogene

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource

0921-4534

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Physics

Electronic Resource