No abstract

The conventional approach to preserving the confidentiality of health records aggregates all records within a geographical area that has a population large enough to ensure prevention of disclosure. Though this approach normally protects the privacy of individuals, the use of such aggregated data limits the types of research one can conduct and makes it impossible to address many important health problems. In this paper we discuss the design and implementation of geographical masks that not only preserve the security of individual health records, but also support the investigation of questions that can be answered only with some knowledge about the location of health events. We describe several alternative methods of masking individual-level data, evaluate their performance, and discuss both the degree to which we can analyse masked data validly as well as the relative security of each approach, should anyone attempt to recover the identity of an individual from the masked data. We conclude that the geographical masks we describe, when appropriately used, protect the confidentiality of health records while permitting many important geographically-based analyses, but that further research is needed to determine how the power of tests for clustering or the strength of other associative relationships are adversely affected by the characteristics of different masks.

The conventional approach to preserving the confidentiality of health records aggregates all records within a geographical area that has a population large enough to ensure prevention of disclosure. Though this approach normally protects the privacy of individuals, the use of such aggregated data limits the types of research one can conduct and makes it impossible to address many important health problems. In this paper we discuss the design and implementation of geographical masks that not only preserve the security of individual health records, but also support the investigation of questions that can be answered only with some knowledge about the location of health events. We describe several alternative methods of masking individual-level data, evaluate their performance, and discuss both the degree to which we can analyse masked data validly as well as the relative security of each approach, should anyone attempt to recover the identity of an individual from the masked data. We conclude that the geographical masks we describe, when appropriately used, protect the confidentiality of health records while permitting many important geographically-based analyses, but that further research is needed to determine how the power of tests for clustering or the strength of other associative relationships are adversely affected by the characteristics of different masks.

SUMMARY. To test the hypothesis that atherosclerosis impairs endothelium-dependent vascular relaxation, we examined the effect of the endothelium-dependent vasodilators acetylcholine and thrombin and the endothehum-independent vasodilator nitroglycerin on iliac arteries from normal cynomolgus monkeys and cynomolgus monkeys with diet-induced atherosclerosis. Rings of iliac artery were suspended in organ chambers at their optimal length for generating tension. After preconstriction with prostaglandin F2,,, cumulative concentration-response curves to acetylcholine, thrombin, and nitroglycerin were examined The presence of endothehum was confirmed in each vessel by scanning electron microscopy. Atherosclerotic vessels showed morpholigic evidence of moderate to severe atherosclerosis. Acetylcholine produced a maximal relaxation of 65 ± 10% in the normal group and 27 ± 10% in atherosclerotic vessels (P < 0 05). Thrombin (10 0 U/ml) produced relaxation of 39 ± 9% in the normal group and 13 ± 7% in atherosclerotic iliac arteries (P < 0.05). Nitroglycerin relaxed both normal and atherosclerotic blood vessels to an equal extentmaximal relaxation was 92 ± 4% in normal vessels and 98 ± 2% in atherosclerotic vessels To determine if hypercholesterolemia alone produces an abnormality in endothelium-dependent relaxation, we performed two additional studies First, because veins are exposed to hypercholesterolemia, but do not develop atherosclerosis, we studied relaxation responses to acetylcholine and thrombin in veins from normal monkeys and monkeys with diet-induced atherosclerosis. Veins from normal and atherosclerotic monkeys relaxed to a similar extent upon exposure to the endothelium-dependent vasodilators acetylcholine and thrombin Second, we studied relaxation responses to acetylcholine, thrombin, and nitroglycerin in left circumflex coronary arteries from normal dogs and dogs fed a hypercholesterolemic diet for 4-5 weeks when serum cholesterol levels were elevated (serum cholesterol 442 ± 14 mg/dl), but before the onset of atherosclerosis. The endothelium-dependent vasodilators acetylcholine and thrombin produced equivalent degrees of relaxation in artenes removed from normal and hypercholesterolemic dogs These studies demonstrate that atherosclerosis impairs endothelium-dependent relaxation in primate iliac arteries, and that this impairment is not due to a generalized defect in the endothelium caused by hypercholesterolemia, but requires the presence of atherosclerosis (Che Res 58: 783-789, 1986)

We examined effects of hypercholesterolemia and atherosclerosis on vasoconstrictor responses to norepinephrine and serotonin. Responses were compared in normal, atherosclerotic, and hypercholesterolemic but non-atherosclerotic cynomolgus monkeys. The hindlimb was perfused at constant flow so that changes in perfusion pressure indicated changes in vascular resistance. We measured the pressure gradient from the iliac to the dorsal pedal artery so that responses of the large artery segment could be determined. Serotonin decreased total hindlimb resistance in normal and hypercholesterolemic monkeys, but increased total resistance in atherosclerotic monkeys. There was a greater than 10-fold increase in constrictor responses of large arteries to serotonin in atherosclerotic monkeys, compared with normal and hypercholesterolemic monkeys. In contrast, we found that vasoconstrictor responses to norepinephrine are normal in atherosclerotic monkeys and increased in hypercholesterolemic monkeys prior to development of atherosclerosis. Hypercholesterolemia augmented responses of small vessels to norepinephrine. We conclude that, during early stages of hypercholesterolemia in cynomolgus monkeys, vasoconstrictor responses to norepinephrine are increased in small vessels. At a later stage, as atherosclerosis develops, responses to norepinephrine return to normal, but vasoconstrictor effects of large arteries to serotonin are greatly potentiated.

No abstract

Atherosclerosis results in impaired relaxation to acetylcholine, thrombin, and the calcium ionophore A23187, all agents that require the presence of endothelium. We now report that dietary treatment of atherosclerosis in monkeys not only produces morphological improvement of the atherosclerotic lesion but restores endothelium-dependent vascular relaxation to normal. ]Because the intima remains thickened after regression of atherosclerosis, these studies suggest that intimal thickening which is present in both atherosclerotic vessels and after regression of atherosclerosis does not prevent the endothelium-derived relaxing factor from reaching the underlying vascular smooth muscle.

Vasa vasorum are present in the middle and outer layers of media in the thoracic aorta of dogs and humans. To examine the role of vasa vasorum in nourishment of the aorta, we ligated four contiguous pairs of intercostal arteries in anesthetized dogs. These arteries are the source of vasa to the descending aorta but not the aortic arch. Blood flow through vasa vasorum was measured with microspheres. Acute intercostal ligation did not reduce conductance in the aortic arch but reduced conductance in the middle third of the descending aorta from 7 +/- 1 to 3 +/- 0.7 (SE) ml.min-1.100 g-1.mmHg-1 (P less than 0.05). After intercostal ligation, infusion of adenosine (5 mumol.kg-1.min-1 iv) increased conductance in the aortic arch 3- to 4-fold but did not increase conductance in the descending aorta. Six to ten days after intercostal ligation, conductance in the middle third of the descending aorta remained low. Vasodilator capacity was partially restored in outer layers of the descending aorta, probably by collateral vessels or formation of new vessels. Morphological changes ranged from broad bands of necrosis to patchy areas of cell loss, primarily in middle layers of descending aorta. We conclude that vasa vasorum are critical in nourishment of aortic media.