Inhalation technique of asthma and COPD patients is poor. In daily practice, community pharmacy-based pharmacists are well suited to significantly supplement doctor-based education in inhalation technique.

In nearly one of five encounters, a direct pharmacist-patient interaction about self-medication revealed relevant DRPs. Having access to patient files including data on prescription and OTC drugs may increase patient safety.

Age-related changes in pharmacokinetics principally affect drug absorption, distribution, metabolism and elimination. Changes in pharmacodynamics are primarily seen in the cardiovascular and neuroendocrine system. Age-dependent changes in the kinetics and dynamics of drugs acting on the cardiovascular system and central nervous system are common, and this review, while by no means exhaustive of the effects of drugs on all organ systems, is reflective of the principles and gives examples of the effects of age on these 2 major systems. While pharmacokinetic changes in the elderly are usually well characterised, pharmacodynamic changes are understood only in the most preliminary way. There has been relatively little research in this area of geriatric clinical pharmacology, and pharmacodynamic changes are still an area of investigation.

Pharmacists in the community pharmacy setting are well suited to identify and resolve DRPs. Ensuring the proper use of both prescription and OTC drugs is one of the basic responsibilities of pharmacists. This specific role of pharmacists within the healthcare system needs to be more fully recognized.

Deregulated activation of the canonical Wnt signalling pathway leads to stabilization of beta-catenin and is critically involved in carcinogenesis by an inappropriate induction of lymphocyte enhancer factor (LEF-1)/beta-catenin-dependent transcription of Wnt target genes. Phosphorylation of the pathway components beta-catenin, Dishevelled, Axin and APC (adenomatous polyposis coli) by glycogen synthase kinase-3beta, CK1 and CK2 is of central importance in the regulation of the beta-catenin destruction complex. Here, we identify CK1 and CK2 as major kinases that directly bind to and phosphorylate LEF-1 inducing distinct, kinase-specific changes in the LEF-1/DNA complex. Moreover, CK1-dependent phosphorylation in contrast to CK2 disrupts the association of beta-catenin and LEF-1 but does not impair DNA binding of LEF-1. Sequential phosphorylation assays revealed that for efficient disruption of the LEF-1/beta-catenin complex, beta-catenin also has to be phosphorylated. Consistent with these observations, CK1-dependent phosphorylation inhibits, whereas CK2 activates LEF-1/beta-catenin transcriptional activity in reporter gene assays. These data are in line with a negative regulatory function of CK1 in the Wnt signalling pathway, where CK1 in addition to the beta-catenin destruction complex at a second level acts as a negative regulator of the LEF-1/beta-catenin transcription complex, thereby protecting cells from development of cancer.