Recently, infertility treatment-related psychological effects are receiving increased attention. However, whether sexual satisfaction is reduced amongst infertile couples remains to be elucidated. In this study, sexual satisfaction of Japanese infertile couples was assessed using a validated questionnaire designed to assess the male and female partner individually, and the couple as a whole for the first time. This study randomly included 170 infertile couples seen at the outpatient clinic and 170 couples that had recently achieved spontaneous pregnancy. All couples were given the Japanese version of the Golombok-Rust Inventory of Sexual Satisfaction (GRISS). In couples aged 35 years or older, the male partners showed significantly worse sexual satisfaction scores than the female partners. Sexual satisfaction also deteriorated with therapeutic interventions, with mental factors affected more than physical factors. Therapeutic interventions such as timed sexual intercourse and assisted reproductive technology were considered emotionally stressful for infertile couples, with sexual satisfaction accordingly lower in this group than in couples achieving spontaneous pregnancy. GRISS successfully evaluated lower sexual satisfaction associated with infertility, and hence is a useful tool for identifying couples whose sexual satisfaction could be enhanced by counselling or other stress-reduction modalities.

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp lthough it has been suggested that oxidative stress plays a causative role in arteriosclerosis, 1,2 aging, 3 heart failure, 4,5 and reperfusion injury during ischemia, 6 the primary role of oxidative stress in the development of each of these pathological situations is unclear. We have documented that N-acetylcysteine, a precursor of glutathione, suppressed ventricular remodeling and arrhythmia in experimental autoimmune myocarditis of rats. 7 Therefore, oxidative stress played a key role in promoting electrical and structural remodeling in a model of myocarditis. Similarly, several reports have demonstrated electrophysiological changes that might be caused by oxidative stress in disease-model animals. 7-11 However, oxidative stress appears with the progression of pathological conditions (eg, inflammation, ischemia, hypertrophy etc), so it is technically difficult to evaluate the effect of hyperoxidative stress separately from other pathological factors in such disease models. As a result, the precise mechanism of the remodeling caused by primary oxidative stress is unclear in these models.In the present study, we designed a rat model of primary hyperoxidative stress without any other structural abnormalities in order to evaluate the role of primary oxidative stress in the promotion of myocardial electrical and structural remodeling. MethodsGlutathione-Depleted Hyperoxidative Rat Model 8-week-old Sprague-Dawley rats (CLEA Japan, Inc, Tokyo, Japan) were treated with L-buthionine-sulfoximine (BSO) (0 or 30 mmol · L -1 · day -1 , control group n=21, BSO group n=18) in drinking water for 14 days. On day 7 and/or 14, the Received October 26, 2010; revised manuscript received January 11, 2011; accepted January 28, 2011; released online April 16, 2011 Time for primary review: 28 days Department of Cardio-Angiology, Kitasato University School of Medicine, Sagamihara, Japan Name of grant: no grant. Mailing address: Sayaka Kurokawa, MD, Department of Cardio-Angiology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara 252-0374, Japan. E-mail: ksayaka@med. Background: Although oxidative stress is considered to promote arrhythmogenic substrates in diseased model animals, it is difficult to evaluate its primary role. In this study, we evaluated the promotion of arrhythmogenic substrates in the primary hyperoxidative state.

Objectives: To analyze the prevalence of systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation and risk factors associated with this condition. Methods: A total of 201 patients who received living-donor kidney transplantation (114 patients with ABO-identical kidney transplantation and 87 patients with ABO-incompatible kidney transplantation) were retrospectively analyzed. Systemic de novo thrombotic microangiopathy was diagnosed clinically according to the presence of thrombocytopenia with microangiopathic hemolytic anemia and pathological findings of thrombotic microangiopathy. Anti-A and anti-B antibodies were purified from human plasma, and these antibodies' bindings to human kidney were investigated in vitro. Results: ABO-incompatible kidney transplantation was a significant risk factor of systemic de novo thrombotic microangiopathy (odds ratio 55.9, 95% CI 1.8-8.9, P < 0.001) after transplantation. Multivariate logistic regression analysis showed that non-use of mycophenolate mofetil, pretreatment immunoglobulin G antibody titer ≥64fold and pretransplant immunoglobulin M antibody titer ≥16-fold were significant risk factors for systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation. Microvascular inflammation of 1-h post-transplant biopsy could be observed more frequently in thrombotic microangiopathy patients than in nonthrombotic microangiopathy patients. Anti-A and anti-B antibodies purified from human plasma showed a strong in vitro reaction against human kidney when the antibody titer was ≥16-fold. Conclusions: Antibody titer should be decreased to ≤16-fold until the day of ABOincompatible kidney transplantation by desensitization therapy including mycophenolate mofetil. The 1-h biopsy results might help to diagnose systemic de novo thrombotic microangiopathy.

No abstract

No abstract