AIM To study the effects of superox- ide anion (O ) on Ca2+ homeostasi and contractility in cultured bovine aortic smooth muscle cell. METHODS Using Fura-2 fluorescence technique to determine Ca2+ level and collagen gel contraction system to analyze muscle contractility. RESULTS ATP (10 ?mol? L-1 )-induced Ca2+ transient was smaller in xanthine oxidase treated cells(X/XO) than control. The mean peak increment of [Ca2+ ]i (△[Ca2+ ], peak) and the time integral of the elevated [Ca2+ ], (∫ △[Ca2+ ]i dt) for 5 min were decreased from (206. 1 ? 10.2) to (147.4 ? 14.7) nmol? L-1, and from (12.2 ?0.5) to (9.8 ? 0.8) ?mol?L-1 .s-1. △ [Ca2+ ], peak induced by thapsigargin(1 ?mol. L- 1 ) in Ca2+ -free solution was not affected by X/XO, but was decreased from (27. 3 ? 1 .0) nmol? L－l to (13 .5 ? 1 .0 ) nmol? L- １ in Ca2+ -containing solution be cause of the activation of CRAC(△［Ｃa2+ ], CRAC). X/XO accelerated the velocity of thapsigargin-induced Ca2+ leak from (78.7 ? 3.4) s to (64.8 ? 4.40) s. Gel contraction area in X/XO-treated cells induced by ATP or thapsigargin (in Ca2+ free solution and in Krebs solution) was decreased from 23.6% ? 4.6% to 7.4% ?0.2%, from 3.5% ?0.6% to － l.0% ? 0.5%, and from 7.9% ? l.4% to － 0.5% ? 0.7%, respectively. CONCLUTION O2- attenuats smooth muscle contraction by impairing some of Ca2+ mobilization pathways.

AIM　To study the effects of superoxide anion (O.2) on Ca2+ homeostasi and contractility in cultured bovine aortic smooth muscle cell. METHODS　Using Fura-2 fluorescence technique to determine Ca2+ level and collagen gel contraction system to analyze muscle contractility. RESULTS　ATP (10 μmol*L-1 )-induced Ca2+ transient was smaller in xanthine oxidase treated cells(X/XO) than control. The mean peak increment of ［Ca2+］i(△［Ca2+］i peak) and the time integral of the elevated ［Ca2+］i(∫△［Ca2+］i dt) for 5 min were decreased from (206.1±10.2) to (147.4±14.7) nmol·L-1,and from (12.2±0.5) to (9.8±0.8) μmol·L-1·s-1. Δ［Ca2+］i peak induced by thapsigargin（1 μmol·L-1 ）in Ca2+-free solution was not affected by X/XO, but was decreased from (27.3±1.0) nmol·L-1 to (13.5±1.0) nmol·L-1 in Ca2+-containing solution because of the activation of CRAC(△［Ca2+］i CRAC). X/XO accelerated the velocity of thapsigargin-induced Ca2+ leak from (78.7±3.4) s to (64.8±4.40) s. Gel contraction area in X/XO-treated cells induced by ATP or thapsigargin (in Ca2+ free solution and in Krebs solution)was decreased from 23.6%±4.6% to 7.4%±0.2%, from 3.5%±0.6% to -1.0%±0.5%, and from 7.9%±1.4% to -0.5%±0.7%, respectively. CONCLUTION　O.2 attenuats smooth muscle contraction by impairing some of Ca2+ mobilization pathways.

A certain period of time has passed since the transition to the General Medicine residency system under the Japanese Medical Specialty Board and Family Medicine specialist training system by the Japan Primary Care Association. We have summarized the needs of residents identified in the survey, and detailed the activities to date and prospects of the Japanese Association of Family Physician Trainees, a self-help support organization, which is an official subcommittee of the Japan Primary Care Association, from the viewpoint of the residents. We believe that this paper will serve as a resource for the training of residents, help guide them under the new system, and help to improve the training system, considering evidence suggesting that information may not be reaching residents who need support.