Health status among elderly Hungarians and Americans

Selected health status data for elderly populations from similar industrial cities-Youngstown, Ohio, USA, and Debrecen, Hungary—were compared. Because of their impoverished health care system, unregulated heavily industrialized society, and unhealthful life-styles Hungarians were hypothesized to have poorer health status than Americans, even after taking into account demographic mediating factors. The study provides a health status baseline for elderly Hungarians shortly after communism's fall in 1989–1990 and shows how great a gap exists between Hungarian health status and that in the West. Hungarians were in much poorer health as measured by functional status, symptomatology, medical condition, depression, and subjective health status. Distinctions persisted when controlling for gender, age, and education. Poverty-level (and income) did not explain health status differences. The paper concludes that Hungary should pay more attention to health promotion, prevention, and primary care, as well as to reforming patient management in hospitals, nursing homes, and home care programs.     

A comparative study of the psychosocial assets of adults with cystic fibrosis and their healthy peers

Psychosocial assets of 37 adults with cystic fibrosis (CF) and 46 of their healthy peers were assessed by mailed questionnaire. Major sociodemographic variables did not differ significantly between the two groups, nor did indices of emotional social support, social network density, self-esteem, or current life satisfaction. This study revealed adults with CF to function on a par with their healthy peers in nearly all respects, a finding at odds with those from uncontrolled studies and which suggests to us that many previous conclusions about the psychosocial health of adults with CF have been unwarranted. Future psychosocial studies involving patients with CF should include control groups and inferences about the effect of these patients' physical illness on their psychosocial health should not be made in the absence of normative data.     

L51P - A BMP2 variant with osteoinductive activity via inhibition of Noggin

Bone morphogenetic proteins (BMP) have to be applied at high concentrations to stimulate bone healing. The limited therapeutic efficacy may be due to the local presence of BMP antagonists such as Noggin. Thus, inhibiting BMP antagonists is an attractive therapeutic option. We hypothesized that the engineered BMP2 variant L51P stimulates osteoinduction by antagonizing Noggin-mediated inhibition of BMP2. Primary murine osteoblasts (OB) were treated with L51P, BMP2, and Noggin. OB proliferation and differentiation were quantified with XTT and alkaline phosphatase (ALP) assays. BMP receptor dependent intracellular signaling in OB was evaluated with Smad and p38 MAPK phosphorylation assays. BMP2, Noggin, BMP receptor Ia/Ib/II, osteocalcin, and ALP mRNA expressions were analyzed with real-time PCR. L51P stimulated OB differentiation by blocking Noggin mediated inhibition of BMP2. L51P did not induce OB differentiation directly and did not activate BMP receptor dependent intracellular signaling via the Smad pathway. Treatment of OB cultures with BMP2 but not with L51P resulted in an increased expression of ALP, BMP2, and Noggin mRNA. By inhibiting the BMP antagonist Noggin, L51P enhances BMP2 activity and stimulates osteoinduction without exhibiting direct osteoinductive function. Indirect osteoinduction with L51P seems to be advantageous to osteoinduction with BMP2 as BMP2 stimulates the expression of Noggin thereby self-limiting its own osteoinductive activity. Treatment with L51P is the first protein-based approach available to augment BMP2 induced bone regeneration through inhibition of BMP antagonists. The described strategy may help to decrease the amounts of exogenous BMPs currently required to stimulate bone healing.     

A calcified coronary artery aneurysm following Kawasaki syndrome]

On the chest X-ray of a 15-year-old patient, a round, egg-shell-like calcification was seen in projection into the left heart border. This finding was caused by a calcified coronary aneurysm following Kawasaki's disease. Although this has been described as a typical change, it is rarely found in daily clinical routine.