Search

To evaluate 2 simple strategies, vitamin D 3 and a home exercise program, in functional recovery during the first year after hip fracture. Secondary analysis of a factorial clinical trial. Patients were randomly allocated to 800 IU (standard of care) or 2000 IU vitamin D 3 and a daily instruction of a simple home exercise program (SHEP) or standard physiotherapy alone during acute care. Acute hip fracture patients aged ≥65 years, after hip fracture surgery, admitted to a large hospital in Zurich, Switzerland. Three objective measures of lower extremity function were assessed at baseline and 6 and 12 months, with the Timed Up and Go test (TUG) as the primary endpoint, and knee flexor and extensor strength, and a self-reported physical function score (PF-10) as secondary endpoints. Linear mixed model regression analyses were based on intention to treat, adjusting for baseline function, time, age, sex, and baseline 25-hydroxyvitamin D level. We enrolled 173 patients (79.2% women; mean age 84 years; 77.5% living at home). A significant interaction was found between vitamin D 3 dose and SHEP for TUG (P =.045). Thus, findings compared the standard of care reference arm with 800 IU vitamin D 3 without SHEP to 3 interventions arms (800 IU vitamin D 3 +SHEP; 2000 IU vitamin D 3 without SHEP; 2000 IU vitamin D 3 +SHEP). For TUG, over 12 months the 800 IU vitamin D 3 +SHEP group performed significantly better than the standard-of-care group (13.8 vs 19.5 seconds; P =.01). Findings for knee flexor strength were in line with TUG results and approached significance (P =.07), whereas knee extensor strength and PF-10 did not differ by treatments. For functional recovery after hip fracture, combining home exercise with 800 IU vitamin D 3 is superior to no home exercise or 2000 IU vitamin D 3. None of the interventions improved subjective physical functioning. [ABSTRACT FROM AUTHOR]

A 30 cM broad genomic region on the long arm of chromosome 10 at 80 cM shows significant and consistent linkage with AD and with plasma concentration of the beta-amyloid peptide 1-42 (Abeta42). The PLAU gene, which is involved in the production and degradation of Abeta42, maps to that region and is therefore a strong positional candidate for association with sporadic AD. We analyzed the non-synonymous single nucleotide polymorphism (SNP) rs2227564 in two independent case-control series from Switzerland and Greece and investigated the influence of this SNP on cognition in elderly individuals. Because PLAU modulates the cleavage of the amyloid precursor protein (APP) and the degradation of Abeta, we also determined the levels of Abeta in the brain, plasma and in the cerebrospinal fluid (CSF). We found no evidence for association of this SNP with AD or with AD-related traits such as beta-amyloid load in the medial temporal lobe or Abeta42 concentration in the CSF and in plasma. Our findings do not support a major role of PLAU polymorphisms as susceptibility factors for AD and suggest that large-scale association studies which combine genetic information from populations with similar genetic background might prevent the generation of spurious associations. Although PLAU may be pathophysiologially related to AD, the contribution of common genetic variants of this gene to the risk for developing AD is likely to be low., (Copyright 2004 Wiley-Liss, Inc.)