No abstract

MCP-1 (monocyte chemotactic protein-1) is a CC

No abstract

The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) and vasopressin infusion. Tachygastria was expressed as the signal percent >4.5 cycles/min. Vection evoked nausea scores of 2.6 +/- 0.2 (0 = none to 3 = severe) in 10 subjects with increases in tachygastric activity (15 +/- 2 to 45 +/- 3%) and plasma vasopressin (4.5 +/- 1.5 to 8.4 +/- 2.5 pg/ml) that were blocked by atropine but not indomethacin. Four asymptomatic subjects had no tachygastria or vasopressin release. Vasopressin at 0.2 U/min (plasma level = 322.1 +/- 10.3 pg/ml) evoked nausea (2.6 +/- 0.4) and increases in tachyarrhythmic activity (41 +/- 5%) that were blunted by atropine but not indomethacin. There were no differences in nausea or dysrhythmias with vasopressin infusion in subjects who noted nausea during vection versus those who did not. To conclude, vection evokes nausea, dysrhythmias, and vasopressin release in motion sickness-susceptible humans via cholinergic prostaglandin-independent pathways. Supraphysiological vasopressin infusions evoke nausea and dysrhythmias by similar pathways to equal degrees in motion sickness-susceptible and -resistant subjects. Thus central but not peripheral actions of vasopressin may contribute to nausea and slow wave disruption with vection. Blunting of both the release and action of vasopressin by atropine may explain its beneficial action in motion sickness.

The introduction of coronary stents marked a major turning point in the practice of interventional cardiology. Whereas the efficacy of balloon angioplasty was challenged both by immediate mechanical complications and by a high incidence of restenosis, coronary stents offered cardiologists a means by which to not only augment immediate procedural success, but also to reduce the incidence of restenosis following coronary intervention. However, despite technological advances and an improved understanding of the restenotic process, the overall rate of in-stent restenosis following bare metal stent implantation remains high. Although the introduction of drug-eluting stents has further reduced the incidence of restenosis, the "real-world" application of drug-eluting stents in increasingly complex lesion and patient subsets has given way to the even greater clinical challenge of managing drug-eluting stent restenosis. Although the standard treatment of bare metal stent restenosis typically involves placement of a drug-eluting stent, the optimal therapeutic approach to drugeluting stent restenosis remains less defined. The issue of in-stent restenosis (especially following implantation of a drug-eluting stent) remains a clinical challenge, and investigation into therapeutic options remains ongoing. As technology evolves, such investigation will likely incorporate novel approaches including drug-coated balloons novel stent designs.