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Although exercise oscillatory ventilation has emerged as a potent independent risk factor for adverse prognosis in heart failure, it is not well known whether cardiac rehabilitation can improve oscillatory ventilation. In this study, we investigated the magnitude of oscillations in ventilation before and after cardiac rehabilitation in chronic heart failure patients with exercise oscillatory ventilation. Cardiac rehabilitation (5-month program) was performed in 26 patients with chronic heart failure who showed an oscillatory ventilation pattern during cardiopulmonary exercise testing (CPX). After the 5-month rehabilitation program was completed, the patients again underwent CPX. To determine the magnitude of oscillations in ventilation, the amplitude and cycle length of the oscillations were calculated and compared with several other parameters, including biomarkers that have established prognostic value in heart failure. At baseline before cardiac rehabilitation, both oscillation amplitude ( R = 0.625, P < 0.01) and cycle length ( R = 0.469, P < 0.05) were positively correlated with the slope of minute ventilation vs. carbon dioxide production. Plasma BNP levels were positively correlated with amplitude ( R = 0.615, P < 0.01) but not cycle length ( R = 0.371). Cardiac rehabilitation decreased oscillation amplitude ( P < 0.01) but failed to change cycle length. The change in amplitude was positively correlated with the change in BNP levels ( R = 0.760, P < 0.01). Multiple regression analysis showed that only the change in amplitude was an independent predictor of the change in BNP levels ( R = 0.717, P < 0.01). A 5-month cardiac rehabilitation program improves exercise oscillatory ventilation in chronic heart failure patients by reducing the oscillation amplitude. This effect is associated with a reduction of plasma BNP levels, potentially contributing to an improvement of heart failure. [ABSTRACT FROM AUTHOR]

We set up a cohort of HIV-infected, asymptomatic Japanese patients with hemophilia for follow-up study in 1995. All subjects who had been infected with HIV-1 for more than 10 years met the criteria for long-term nonprogressors (LTNPs) at the time of entry; however, some of them later developed lymphopenia and required antiretroviral treatment during five more years of observation. In this study, we investigated the impacts of the CCL3L1 dose on the long-term prognosis in the subjects with chronic HIV-1 infection. We collected genomic DNA from 95 long-term survivors including 48 nonprogressors and 47 subjects receiving antiretroviral treatment. The distributions of CCL3L1 copy number significantly differed between the 95 HIV-1-infected subjects with hemophilia and 205 controls. Average copy number of CCL3L1 in the HIV-1-infected subjects was significantly lower than in control (5.00 ± 0.22 vs 3.35 ± 0.24, p < 0.001). Moreover, the subjects possessing two or less copies of CCL3L1 had significantly higher risk of acquiring HIV-1. However, CCL3L1 copy number variations had no significant effect on the disease progression among the LTNP subjects who had been afflicted with chronic HIV-1 infection for more than 15 years, when compared between nonprogressors and patients under treatment (3.68 ± 0.37 vs 3.02 ± 0.29, ns). Furthermore, variations in the CCL3L1 copy number had little effect on the levels of HIV-1 load among them. We conclude that variation in the CCL3L1 copy number is apparently not a factor that determines the prognosis of chronic HIV-1 infection, even though it is linked to HIV-1 susceptibility. [ABSTRACT FROM AUTHOR]

Buerger disease (BD) and Takayasu arteritis (TA) are rare vascular disorders. Although their etiology and pathogenesis have not been elucidated, several studies have suggested the involvement of innate immunity. Myeloid differentiation primary-response protein 88 (MyD88) is a key signaling adaptor for all Toll-like receptors, which have a central role in innate immunity. In the present study, we evaluated the association of MyD88 with BD and TA. We conducted case-control studies in Japanese populations composing of 131 BD cases, 90 TA cases and 270 healthy controls to be genotyped for a single nucleotide polymorphism rs7744 A>G in the 3′-untranslated region of MyD88 gene. The frequency of GG genotype was significantly lower in the BD patients than in the controls (6.9 vs 15.9%, P=0.011, odds ratio=0.39, 95% confidence interval; 0.19, 0.81), although there was no significant difference in the genotype frequencies between the TA patients and controls. It was suggested that MyD88 may confer resistance to BD in Japanese. Because this is the first report of the association between MyD88 and BD, replication studies in other cohorts are required. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) and stroke are the major health problems in many countries because of their increasing prevalence and high mortality. It is well known that CAD and stroke are based on atherosclerosis and shared environmental and genetic risk factors. Recently, an association of a functional sequence variation −154G>A in the angiotensin receptor-like 1 (AGTRL1) with a susceptibility to stroke was reported. In this study, we investigated a total of 1479 CAD cases and 2062 controls from the Japanese and Korean populations to validate the association of AGTRL1 with CAD. However, we obtained no evidence of the association in both the Japanese (odds ratio (OR)=0.95, 95% confidence interval (CI); 0.82–1.10, P=0.47, allele count model) and Korean (OR=0.90, 95% CI; 0.77–1.05, P=0.18, allele count model) populations. In addition, there was no trend of association between the risk allele and severity of coronary atherosclerosis. These data suggested that AGTRL1 did not contribute much to the atherosclerosis of the coronary artery. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) has become a major health problem in many countries. Recent genome-wide association studies have identified the association between rs1333049 on chromosome 9p21 and susceptibility to CAD in Caucasoid populations. In this study, we evaluated the associations of rs1333049 with CAD in Japanese (604 patients and 1,151 controls) and Koreans (679 patients and 706 controls). We found a significant association in both Japanese [odds ratio (OR) = 1.30, 95% confidence interval (CI); 1.13–1.49, p = 0.00027, allele count model] and Koreans (OR = 1.19, 95% CI; 1.02–1.38, p = 0.025, allele count model). These observations demonstrated that chromosome 9p21 was the susceptibility locus for CAD also in East Asians. [ABSTRACT FROM AUTHOR]