Intergenerational solidarity and the family–welfare state balance

The article addresses the strength and character of intergenerational family solidarity under different family cultures and welfare state regimes in order to answer the following two questions: (1) Is intergenerational solidarity stronger under the more collectivist southern family tradition than under the more individualist northern tradition? (2) Is more generous access to social care services a risk or a resource for family care? These questions are explored with data from the OASIS project, a comparative study among the urban populations aged 25+ (n=6,106) in Norway, England, Germany, Spain, and Israel. The findings indicate that the welfare state has not crowded out the family in elder care, but has rather helped the generations establish more independent relationships. Intergenerational solidarity is substantial in both the northern and southern welfare state regimes, and seems to vary in character more than in strength.     

Graded blood pressure reduction in hypertensive outpatients associated with use of a device to assist with slow breathing

To study the effects of device-guided breathing on office systolic blood pressure (SBP), five centers randomized 149 untrained hypertensives (50% male, age 59+/-10 years, baseline blood pressure 150+/-9/86+/-9 mm Hg, 77% taking drug therapy). One half received a device to guide slow breathing; all received a home blood pressure monitor and only simple, written instructions. The changes in office SBP (adjusted for office-to-home difference in baseline SBP and accumulated time spent in slow breathing, guided and measured by the device) were significantly (p<0.001 for trend) correlated with accumulated time spent in slow breathing. Greater decreases in SBP (-15.0+/-1.8 vs. -7.3+/-1.9 mm Hg) were observed for those who spent more (vs. less) than 180 minutes over 8 weeks in slow breathing, as well as those who just monitored their blood pressure at home (-9.2+/-1.6 mm Hg). Thus, even without training, hypertensive patients who receive a device to guide slow breathing significantly lowered their office SBP if the total time spent in slow breathing over 8 weeks exceeded a "threshold" value of 180 minutes.     

ACE inhibition limits chronic injury of kidney transplant even with treatment started when lesions are established

BACKGROUND: Inhibition of the renin-angiotensin system (RAS) prevents development of chronic allograft dysfunction in experimental animals. Whether this therapeutic approach is effective even if started when signs of allograft nephropathy are already manifested has not been investigated. METHODS: To address this issue, we studied the effect of a late treatment with the angiotensin-convertine enzyme (ACE) inhibitor trandolapril in the Fisher 344 to Lewis rat kidney transplant model. Seven months after transplant a renal biopsy was done for graft histology examination. Thereafter rats received either no treatment (allograft-none) or trandolapril until sacrifice at month 13. RESULTS: All animals were alive at the end of the study with the exception of a rat in the untreated group that died of renal insufficiency at day 292. Despite the fact that the grafts had already signs of structural injury and function impairment at the time treatment was stated, trandolapril completely restored renal function to baseline pretransplant values. Trandolapril also halted the progression of glomerular damage and suppressed intragraft T-lymphocyte infiltration and reduced the expression of the chemokine monocyte chemoattractant protein-1 (MCP-1). However, trandolapril had no direct effect on T cell function, since in vivo treatment did not modify recipient T-cell alloreactivity against donor antigens. CONCLUSION: These findings provide the basis for a novel treatment intervention with RAS blockade that, together with pharmacologic inhibition of the immune response, could interrupt progression of chronic allograft dysfunction and injury.     

Add-on anti-TGF-beta antibody to ACE inhibitor arrests progressive diabetic nephropathy in the rat

Renin-angiotensin system (RAS) inhibitors are effective in reducing renal disease progression in early diabetic nephropathy, but they provide imperfect protection at a later stage. Due to the pivotal role of transforming growth factor-beta (TGF-beta) in the pathogenesis of diabetic kidney disease, this study tested the effect of simultaneously interrupting TGF-beta and angiotensin II on disease progression in diabetic rats with overt nephropathy. Diabetes was induced by streptozotocin injection in uninephrectomized rats. Diabetic rats received murine (1D11) or human (CAT-192) anti-TGF-beta monoclonal antibodies alone or in combination with lisinopril, 13C4 irrelevant murine antibody, saline or lisinopril from month 4 (when animals had proteinuria) to month 8. Normal animals served as controls. Systolic BP increase was controlled by single treatments and even more by the combined therapies. 1D11 and lisinopril kept proteinuria at levels numerically lower than irrelevant antibody and saline, while CAT-192 was ineffective. The addition of either TGF-beta antibody to lisinopril normalized proteinuria. Consistent results were obtained for glomerulosclerosis and tubular damage, which were abrogated by the combined therapy. Interstitial volume expansion and infiltration of lymphocytes/macrophages were limited by 1D11 and lisinopril and further reduced by their combination. The increase of type III collagen in the renal interstitium was partially attenuated by 1D11 and lisinopril while normalized by their combination. It is concluded that anti-TGF-beta antibody when added to a background of chronic angiotensin-converting enzyme (ACE) inhibition fully arrests proteinuria and renal injury of overt diabetic nephropathy, providing a novel route to therapy and remission of disease for diabetic patients who do not respond to RAS inhibition.     

Pathology of the heart in the tenth decade

The pathology of the heart was studied in 60 patients dying in their tenth decade in a general hospital. The severity of coronary atherosclerosis and the incidence of ischaemic heart disease was lower than in younger geriatric patients. The incidence of minor ;aging' changes was similar to that in younger patients with the exception of mitral valve atheroma where the increase with aging continued into the tenth decade. Marked nodular thickening of the tricuspid valve was seen only in males. Over half the systolic murmurs heard were associated with mitral valve abnormalities and not with aortic valve changes. Multiple cardiac pathology was more frequent than in younger patients but its association with failure was much less striking. It is concluded that resistance to the development of coronary atherosclerosis and to failure being precipitated by the multiple minor cardiac abnormalities associated with aging are important factors in attaining extreme longevity.