Triply bridged dinuclear ruthenium complexes bearing alkylbis(2-pyridylmethyl)amine in the mixed-valence state of Ru(ii)-Ru(iii).

Triply halogeno and methoxido-bridged dinuclear ruthenium complexes bearing a tridentate ancillary ligand, alkylbis(2-pyridylmethyl)amine (alkyl, ethyl and benzyl), in the Ru(ii)-Ru(iii) mixed-valence state were synthesized by reduction reactions of the trichloridoruthenium(iii) complex, fac-[RuIIICl3(ebpma)], followed by chlorido-substitution and oxidation reactions in air. The conversion of the bridging ligands of the diruthenium complexes was also made possible through reduction of the dinuclear core. The electronic structures of the mixed-valence state were investigated by electron spin resonance (ESR), X-ray crystallography, electrochemical measurements and UV-vis-near infrared (NIR) spectroscopy. The mixed-valence state of all the triply bridged complexes was stable and classified as Class III.

Roles of basophils and mast cells infiltrating the lung by multiple antigen challenges in asthmatic responses of mice.

BACKGROUND AND PURPOSE: Mast cell hyperplasia has been observed in the lungs of mice with experimental asthma, but few reports have studied basophils. Here, we attempted to discriminate and quantify mast cells and basophils in the lungs in a murine asthma model, determine if both cells were increased by multiple antigen challenges and assess the roles of those cells in asthmatic responses. EXPERIMENTAL APPROACH: Sensitized Balb/c mice were intratracheally challenged with ovalbumin four times. Mast cells and basophils in enzymatically digested lung tissue were detected by flow cytometry. An anti-FcεRI monoclonal antibody, MAR-1, was i.p. administered during the multiple challenges. KEY RESULTS: The numbers of both mast cells (IgE(+) C-kit(+) ) and basophils (IgE(+) C-kit(-) CD49b(+) ) increased in the lungs after three challenges. Treatment with MAR-1 completely abolished the increases; however, a late-phase increase in specific airway resistance (sRaw), and airway eosinophilia and neutrophilia were not affected by the treatment, although the early-phase increase in sRaw was suppressed. MAR-1 reduced antigen-induced airway IL-4 production. Basophils infiltrating the lung clearly produced IL-4 after antigen stimulation in vitro; however, histamine and murine mast cell protease 1 were not increased in the serum after the challenge, indicating that mast cell activation was not evoked. CONCLUSION AND IMPLICATIONS: Both mast cells and basophils infiltrated the lungs by multiple intratracheal antigen challenges in sensitized mice. Neither mast cells nor basophils were involved in late-phase airway obstruction, although early-phase obstruction was mediated by basophils. Targeting basophils in asthma therapy may be useful for an early asthmatic response.

[From school of community: transition services and career education for individuals with developmental disabilities].

This article examines the theory and practice relating to transition services and career education for individuals with developmental disabilities in Japan. The article is also intended to guide future enactment and social services that affect life-cycle transitions.

Treatment of hyperthyroidism with a small single daily dose of methimazole: a prospective long-term follow-up study.

A prospective long-term follow-up study was performed with conventional divided doses (group C: 10 mg 3 times daily, N = 58) and a small single daily dose (group S: 15 mg once daily, N = 54) of methimazole (MMI) for the treatment of Graves' hyperthyroidism. Within 8 weeks, almost 80% of the patients in both groups became euthyroid. The mean time required to achieve a euthyroid state was 5.6 +/- 2.7 weeks in group C and 5.8 +/- 3.1 in group S. TSH binding inhibitor immunoglobulin (TBII) levels before therapy were 44.2 +/- 22.7% and 47.1 +/- 23.9% in group C and group S, respectively. A similar gradual fall in TBII levels was observed in both groups over a two-year period of treatment. MMI doses were gradually reduced to a maintenance dose (5 mg daily) after the patients became euthyroid. The patients were treated for 28 +/- 9 months and were followed up after therapy was stopped (observation period in patients who remained in remission was 12-130 (75 +/- 34) months and the interval to relapse in recurred cases was 1-98 (20 +/- 27) months). The rates of recurrence in group C were 41% at 1 yr, 54% at 2 yrs, 56% at 4 yrs and 61% at 6 yrs. In group S, these were 44%, 53%, 56% and 63%, respectively. No differences between relapse rates were observed with the two different dosage regimens. Adverse effects occurred more frequently in group C patients (24%) than in group S patients (13%). These results show that there is no difference in the clinical and immunological course or in the long-term remission rate of Graves' hyperthyroidism when the treatment is initiated with either a small single daily dose (15 mg) or the conventional regimen (10 mg 3 times daily).

Primary aldosteronism with bilateral multiple aldosterone-producing adrenal adenomas.

A 41-year-old woman developed primary aldosteronism due to bilateral multiple aldosterone-producing adenomas (APA). She was suspected to have idiopathic hyperaldosteronism (IHA) 7 years previously. Although preoperative data suggest APA and IHA was suspected in a postoperative microscopic specimen, a definite clinical diagnosis could not be made. Cytochrome P-450 and other enzymes involved in aldosterone synthesis were found in the tumor portions but not in the zona glomerulosa of attached adrenals, which histopathologically showed "paradoxical hyperplasia". This was a rare case of bilateral multiple APA, which could be differentiated from IHA by immunohistochemical analysis of adrenal steroidogenic enzymes.

Graves' hyperthyroidism following transient thyrotoxicosis during interferon therapy for chronic hepatitis type C.

We report a case of Graves' hyperthyroidism induced by long-term interferon (IFN) therapy. A 52-year-old woman suffered from chronic active hepatitis type C and was treated with a total of 456 x 10(6) units of IFN-alpha for 23 weeks. During the 12th week of treatment she showed transient thyrotoxicosis. One week after the termination of IFN therapy, TSH-receptor antibodies became positive and subsequently she showed Graves' hyperthyroidism. This case showed sequential manifestation from transient thyrotoxicosis to the appearance of TSH-receptor autoantibodies, and then the occurrence of Graves' hyperthyroidism during IFN therapy. The course of this case may be useful in the understanding of the pathogenesis of autoimmune hyperthyroidism.

Adrenocorticotropic hormone-independent bilateral adrenocortical macronodular hyperplasia: a case report and immunohistochemical studies.

A 55-year-old woman developed Cushing's syndrome due to ACTH-independent bilateral adrenocortical macronodular hyperplasia. Plasma ACTH was undetectable, and was not stimulated by administration of metyrapone, CRH, or insulin. Hypercortisolism was not suppressed by a high dose of dexamethasone, but was responsive to ACTH. Both adrenal glands were enlarged with a total weight of 200 g, and contained multiple nodules composed of two cell types (large clear cells and small compact cells). In immunohistochemical studies, P450c17 immunoreactivity was predominantly observed in small compact cortical cells, while that of 3 beta HSD was observed exclusively in large clear cortical cells. This pattern of expression of steroidogenic enzymes as well as histological and clinical features is considered to be unique to ACTH-independent bilateral adrenocortical macronodular hyperplasia.