Abstract-Hypertriglyceridemia may contribute to the development of atherosclerosis by increasing expression of cell adhesion molecules (CAMs). Although the cellular expression of CAMs is difficult to assess clinically, soluble forms of CAMs (sCAMs) are present in the circulation and may serve as markers for CAMs. In this study, we examined the association between sCAMs and other risk factors occurring with hypertriglyceridemia, the effect of triglyceride reduction on sCAM levels, and the role of soluble vascular cell adhesion molecule-1 (sVCAM-1) in monocyte adhesion in vitro. Compared with normal control subjects (nϭ20), patients with hypertriglyceridemia and low HDL (nϭ39) had significantly increased levels of soluble intercellular adhesion molecule-1 (sICAM-1) (316Ϯ28.8 versus 225Ϯ16.6 ng/mL), sVCAM-1 (743Ϯ52.2 versus 522Ϯ43.6 ng/mL), and soluble E-selectin (83Ϯ5.9 versus 49Ϯ3.6 ng/mL). ANCOVA showed that the higher sCAM levels in patients occurred independently of diabetes mellitus and other risk factors. In 27 patients who received purified n-3 fatty acid (Omacor) 4 g/d for Ն7 months, triglyceride level was reduced by 47Ϯ4.6%, sICAM-1 level was reduced by 9Ϯ3.4% (Pϭ.02), and soluble E-selectin level was reduced by 16Ϯ3.2% (PϽ.0001), with the greatest reduction in diabetic patients. These results support previous in vitro data showing that disorders in triglyceride and HDL metabolism influence CAM expression and treatment with fish oils may alter vascular cell activation. In a parallel-plate flow chamber, recombinant sVCAM-1 at the concentration seen in patients significantly inhibited adhesion of monocytes to interleukin-
This study evaluated the effectiveness of nondieting versus dieting treatments for overweight, binge-eating women. Participants (N = 219) were randomly assigned to 1 of 3 groups: diet treatment (DT), nondiet treatment (NDT), or wait-list control (WLC). DT received a balanced-deficit diet reinforced with behavioral strategies. NDT received therapy designed to help participants break out of their dieting cycles. Treatment in both conditions was administered in weekly groups for 6 months, followed by 26 biweekly maintenance meetings, for a total of 18 months of contact. At 6 months posttreatment, DT lost 0.6 kg while NDT gained 1.3 kg. Both treatment groups reduced their Binge Eating Scale scores significantly more than WLC. At 18-month follow-up, both treatment groups experienced weight gain but maintained similar reductions in binge eating. Results indicate that neither intervention was successful in producing short- or long-term weight loss. Therapist biases, which may have affected treatment integrity, and other methodological issues are discussed in relation to the small weight losses achieved.
LM, CRP, and exercises are all effective interventions; patient education plus the sham maneuver, however, had some beneficial effect. These results support two possible mechanisms of BPPV: displaced otoconia and a neural mechanism affecting interpretation of semicircular canal signals.
This scale has good face validity, high internal consistency, and high test-retest reliability. It may be useful for evaluating functional limitation and perceived handicap or disability before and after intervention and for helping patients become more realistic in understanding their own capabilities.
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