Simulation studies for the evaluation of health information technologies: experiences and results.

It is essential for new health information technologies (IT) to undergo rigorous evaluations to ensure they are effective and safe for use in real-world situations. However, evaluation of new health IT is challenging, as field studies are often not feasible when the technology being evaluated is not sufficiently mature. Laboratory-based evaluations have also been shown to have insufficient external validity.

Growth hormone increases the proliferation of existing cardiac myocytes and the total number of cardiac myocytes in the rat heart.

Objective: Growth hormone (GH) is known to induce growth of the normal rat heart. Whether this growth is due solely to hypertrophy of the cardiac myocytes or whether a concomitant hyperplasia of the cardiac myocytes also takes place is currently not known. Therefore, the aim of the present study was to investigate whether GH induces hyperplasia in the left ventricle (LV) of sexually mature rats.

[Laboratory animal asthma in research workers].

Working with laboratory animals in research is correlated with a high risk of developing laboratory animal allergy, and 5-40% of researchers exposed to animals develop an allergy within the first year. We describe three cases of asthmatic allergy in the same research group within a brief period of time. The research facility was an old hospital building which had not been adequately rebuilt to support animal facilities.

Extracellular calcium sensing in rat aortic vascular smooth muscle cells.

Extracellular calcium (Ca(2+)(o)) can act as a first messenger in many cell types through a G protein-coupled receptor, calcium-sensing receptor (CaR). It is still debated whether the CaR is expressed in vascular smooth muscle cells (VSMCs). Here, we report the expression of CaR mRNA and protein in rat aortic VSMCs and show that Ca(2+)(o) stimulates proliferation of the cells.

Increased natriuretic peptide receptor A and C gene expression in rats with pressure-overload cardiac hypertrophy.

Both atrial (ANP) and brain (BNP) natriuretic peptide affect development of cardiac hypertrophy and fibrosis via binding to natriuretic peptide receptor (NPR)-A in the heart. A putative clearance receptor, NPR-C, is believed to regulate cardiac levels of ANP and BNP. The renin-angiotensin system also affects cardiac hypertrophy and fibrosis.

Expression profiling reveals differences in metabolic gene expression between exercise-induced cardiac effects and maladaptive cardiac hypertrophy.

While cardiac hypertrophy elicited by pathological stimuli eventually leads to cardiac dysfunction, exercise-induced hypertrophy does not. This suggests that a beneficial hypertrophic phenotype exists. In search of an underlying molecular substrate we used microarray technology to identify cardiac gene expression in response to exercise.

Cyclin D2 induces proliferation of cardiac myocytes and represses hypertrophy.

The myocytes of the adult mammalian heart are considered unable to divide. Instead, mitogens induce cardiomyocyte hypertrophy. We have investigated the effect of adenoviral overexpression of cyclin D2 on myocyte proliferation and morphology.

Involvement of cyclin D activity in left ventricle hypertrophy in vivo and in vitro.

Objective: Cardiac hypertrophy is induced by a number of stimuli and can lead to cardiomyopathy and heart failure. Present knowledge suggests that cell-cycle regulatory proteins take part in hypertrophy. We have investigated if the D-type cyclins are involved in cardiac hypertrophy.