Evidence against the involvement of chronic cerebrospinal venous abnormalities in multiple sclerosis. A case-control study.

Objective: Multiple sclerosis (MS) is a chronic neurodegenerative disease of the CNS. Recently a controversial vascular hypothesis for MS, termed chronic cerebrospinal venous insufficiency (CCSVI), has been advanced. The objective of this study was to evaluate the relative prevalence of the venous abnormalities that define CCSVI.

Analgesic targets: today and tomorrow.

Pain is recognized as a multifactorial sensory experience that is wholly unpleasant. It can vary in intensity from mild to severe and its duration can be anything from transient to persistent. Today we know so much more about the peripheral nociceptor as the primary detection apparatus for painful stimuli.

Inhibition of COX pathway in experimental myocardial infarction.

Release of inflammatory mediators within the ischemic myocardium has long been thought to contribute to myocardial damage and dysfunction. Myocardial infarction (MI) and congestive heart failure (CHF) were induced in rats by ligating the left coronary artery. Animals were treated with the selective cyclooxygenase-2 (COX-2) inhibitor-5,5-dimethyl-3-(3-fluorophenyl1)-4-(4-methyl-sulphonyl-2(5H)-fluranone (DFU), low-, high-dose acetyl salicylic acid (aspirin), or vehicle for 3 months.

Cyclooxygenase-2 (COX-2) in acute myocardial infarction: cellular expression and use of selective COX-2 inhibitor.

Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery.