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A pronounced hippocampal expression of the Protease-activated Receptor 4 (PAR4) has recently been shown. In the current study the authors define the PAR4-associated sub-cellular structures and the influence of global ischaemia on the expression of PAR4. For that purpose the authors performed double labelling with fluorescence immunohistochemistry on tissue from naive and post-ischaemic rats. In naive animals - apart from the expression in granular and pyramidal neurons - there was an intensive lamellar expression of PAR4 in the CA4 region. Further analysis revealed that PAR4 was localised exclusively on mossy fibre axons in CA4 as detected by double-labelling with calbindin D-28k, but there was no overlap with markers of the neuronal cell body, interneurons, and post-synaptic, pre-synaptic and dendritic structures. Three and 14 days post ischaemia, CA1 neurons were degenerated and, consequently, there was no PAR4 signal in the CA1 band. In most other hippocampal structures no change in the PAR4 expression was detectable, with the exception of the CA3 region. Here, the fibre-associated PAR4 signal was diminished and disintegrated post ischaemia. Additionally, a redistribution from the membrane-bound neuronal localisation of PAR4 in control animals to a diffuse localisation all over the cell soma was revealed in the CA3 area 14 days post ischaemia. In conclusion, the current study proves for the first time that PAR4 is localised in mossy fibre axons. The altered expression in CA3 neurons after ischaemia indicates that PAR4 may be involved in post-ischaemic adaptive mechanisms. © 2009 Wiley-Liss, Inc.

Mucociliary clearance (MC) is a key defense mechanism in airways. Smokers and patients with chronic obstructive pulmonary disease (COPD) exhibit modifications in MC, which predisposes these populations to recurrent infections. It is known that ex-smokers with normal lung function may present MC reversing after smoking cessation, but there are no studies that evaluate COPD ex-smokers' MC. Aim: To evaluate and to compare the MC and exhaled carbon monoxide (eCO) in smokers and COPD ex-smokers. Methods: We evaluated 83 subjects, divided in four groups: severe COPD (n=22), moderate COPD (n=19), current smokers (n=20) and nonsmokers (n=22). Severe and moderate COPD patients were ex-smokers (FEV1% = 38[34-43] and 60[53-63], 48[11-100] and 50[40-75] pack/years, respectively). Current smokers presented normal lung function and 40[22-44] pack/years. Nonsmokers were matched for age and sex. Were evaluated eCO levels and MC by saccharin transit time (STT) test. Tests were conducted between 8 and 9 AM with air temperature and relative humidity controlled. Statistical analyses were performed using Kruskal-Wallis test followed by Dunn's test. Results: STT was higher in smokers compared to control group (p=0,006). There was no difference in STT between smokers and COPD groups, but in both groups of COPD STT values were similar to control group. Also, there was no difference in STT between severe and moderate COPD. eCO levels was higher in smokers compared to other three groups (p