ABSTRACT
OBJECTIVES: To examine the acceptability of non-medical, community-based interviewers obtaining blood samples during in-home interviews from low-income study participants. METHODS: Two separate focus groups were conducted, one with ten non-medical community-based interviewers and the other with eight research participants from a low-income population. (Both the interviewers and the research participants had previously taken part in a research project over the course of five years.) RESULTS: Participants and interviewers were comfortable with finger stick blood samples performed in the home. The interviewers felt that adequate training was critical. Participants identified key issues: blood would not be used for other purposes and that the interviewers would be trained to handle blood safely. Both groups felt that it was crucial to communicate the study purpose and results. Recommendations from the focus groups were implemented and the acceptance rate for blood sampling was 99.5% (205/206). CONCLUSION: Proper training of interviewers, organization of supplies, and communication with participants can be combined to maximize acceptance of in-home, finger stick blood sample collection by community-based interviewers among a low-income population.
Subject(s)
Blood Specimen Collection/psychology , Community Health Workers , Health Knowledge, Attitudes, Practice , Patient Participation/psychology , Adult , Black or African American , Chicago , Female , Focus Groups , Home Care Services , Humans , Patient Acceptance of Health Care/psychology , Poverty Areas , Urban PopulationABSTRACT
OBJECTIVE: Although matrix metalloproteinase-9 (MMP-9) has been implicated in atherosclerotic plaque instability, the exact role it plays in the plaque development and progression remains largely unknown. We generated apolipoprotein E (apoE)-deficient (apoE-/-) MMP-9-deficient (MMP-9-/-) mice to determine the mechanisms and the main cell source of MMP-9 responsible for the plaque composition during accelerated atherosclerotic plaque formation. METHODS AND RESULTS: Three weeks after temporary carotid artery ligation revealed that while on a Western-type diet, apoE-/- MMP-9-/- mice had a significant reduction in intimal plaque length and volume compared with apoE-/- MMP-9+/+ mice. The reduction in plaque volume correlated with a significantly lower number of intraplaque cells of resident cells and bone marrow-derived cells. To determine the cellular origin of MMP-9 in plaque development, bone marrow transplantation after total-body irradiation was performed with apoE-/- MMP-9+/+ and apoE-/- MMP-9-/- mice, which showed that only MMP-9 derived from resident arterial cells is required for plaque development. CONCLUSIONS: MMP-9 is derived from resident arterial cells and is required for early atherosclerotic plaque development and cellular accumulation in apoE-/- mice.
Subject(s)
Carotid Artery Diseases/metabolism , Carotid Artery Diseases/pathology , Carotid Artery Injuries/metabolism , Carotid Artery Injuries/pathology , Matrix Metalloproteinase 9/metabolism , Animals , Apolipoproteins E/genetics , Atherosclerosis/metabolism , Atherosclerosis/pathology , Bone Marrow Cells/pathology , Carotid Arteries/enzymology , Carotid Arteries/pathology , Cell Lineage , Ligation , Matrix Metalloproteinase 9/genetics , Mice , Mice, Inbred C57BL , Mice, Mutant StrainsABSTRACT
BACKGROUND: Pharmacological blockade of beta3-integrins inhibits neointimal lesion formation in nonmouse animal models of arterial injury. In contrast, beta3-integrin-deficient (beta3-/-) mice are not protected from neointimal lesion formation after arterial injury. We investigated this discrepancy in beta3-/- and wild-type (beta3+/+) mice using different models of injury. METHODS AND RESULTS: After disruption of the carotid with a transluminal probe, there was no significant difference in neointimal thickening between beta3-/- and beta3+/+ mice. However, after ligation of the carotid without medial disruption, there was reduced neointimal thickening in beta3-/- mice compared with beta3+/+ mice at intervals up to 3 months. Lesion reduction in beta3-/- mice was associated with fewer intimal smooth muscle cells (SMCs) without a difference in SMC apoptosis or proliferation rate compared with beta3+/+ mice, consistent with reduced SMC migration from the media into the intima of beta3-/- mice. Moreover, combined eccentric medial disruption and ligation of the carotid in beta3-/- mice resulted in neointimal lesion formation only at the site of medial disruption. Transplantation of bone marrow cells harvested from beta3+/+ mice into irradiated beta3-/- mice resulted in reduced neointimal lesion formation after carotid ligation injury, confirming the importance of alpha(v)beta3 and not alpha(IIb)beta3 in the attenuated response. CONCLUSIONS: The alpha(v)beta3-integrin mediates intimal SMC accumulation that contributes to neointimal thickening in the setting of arterial ligation.
Subject(s)
Carotid Arteries/pathology , Carotid Artery Injuries/pathology , Carotid Stenosis/etiology , Integrin alphaVbeta3/physiology , Integrin beta3/physiology , Tunica Intima/pathology , Animals , Apoptosis , Bone Marrow Transplantation , Carotid Arteries/metabolism , Carotid Arteries/surgery , Carotid Artery Injuries/etiology , Carotid Stenosis/metabolism , Carotid Stenosis/pathology , Cell Division , Cell Movement , Cells, Cultured/cytology , Cells, Cultured/metabolism , Chemotaxis , Disease Models, Animal , Hyperplasia , Integrin beta3/drug effects , Ligation , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Myocytes, Smooth Muscle/pathology , Platelet Glycoprotein GPIIb-IIIa Complex/physiology , Radiation Chimera , Stress, MechanicalABSTRACT
Although mice deficient in various genes are providing greater insight into the mechanisms of restenosis after angioplasty, there have been limitations with murine models not simulating human vascular disease. To develop a more clinically applicable model of primary atherosclerosis and restenosis following angioplasty of the primary lesion, we fed apolipoprotein E-deficient mice a Western diet and occluded the left common carotid artery for 2 days. Three weeks after flow was restored, the temporarily occluded carotids demonstrated atherosclerotic lesions containing foam cells, cholesterol clefts, necrotic cores, and fibrous capsules. The atherosclerotic carotids in other animals underwent angioplasty with a beaded probe, resulting in plaque and medial layer disruption. Three weeks after angioplasty, although there was significant neointimal lesion formation, the luminal narrowing did not change significantly secondary to overall vessel enlargement (positive remodeling). Neointimal lesions were composed of smooth-muscle cells and extracellular matrix observed adjacent to the original atherosclerotic plaques. Similarly, even at 3 months after the angioplasty the lumen was maintained despite greater neointimal lesion formation caused by progressive positive remodeling. This new murine model of primary atherosclerosis and postangioplasty intimal hyperplasia and remodeling mimics the human disease pattern of postangioplasty intimal hyperplasia. Used in transgenic animals, this model will likely facilitate understanding of the mechanisms of restenosis in humans.
