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Purpose Poor living conditions are posited as an underlying cause of American Indian (AI) infant mortality, which is unusually high in the postneonatal period. We explore whether the effects of neighborhood poverty on AI infant death are identifiable by using observational data. Methods Vital records for infants born between 1990 and 1999 to AI women in a metropolitan area (n = 4751) are linked with tract-level poverty data. A counterfactual framework, an explicit causal contrast study design, and propensity score matching methods were used. For each comparison, we created exchangeable groups by matching infants with the same probability of exposure to poverty when one was exposed and the other was not. Results Our results suggest that neighborhood poverty has little effect on AI infant death outcomes. Importantly, the study design makes transparent the challenge of identifying appropriate analytic comparison groups in studies of neighborhood poverty and health. Conclusions Collecting additional data will likely not overcome the fact that AIs with a high probability of living in poverty rarely reside in low-poverty neighborhoods. Yet, some of them must if a meaningful counterfactual comparison is to be made and the effects of neighborhood poverty on AI infant death are to be identified.

Early “environmental equity” studies claimed hazardous waste facilities (TSDFs) were disproportionately located in minority and disadvantaged communities. Recently, research has challenged such claims. Regardless of conclusions, no national study has evaluated inequity in the siting process or the impact of TSDFs on the demographic composition of communities after TSDFs began operations, or distinguished between TSDF-caused change and general population trends. This article presents findings from the first national tract-level longitudinal study of communities with TSDFs. We find no stark evidence of environmental inequity or disparate impact. Results suggest compositional change in host communities may best be explained by general population trends.

A resonance Raman spectroscopic study of the porcine myoglobin double mutant H64V/V68H has confirmed that the ferric form is bis-histidine ligated, has revealed that the bis-histidine ligation is retained on reduction to the ferrous form, and has demonstrated that CO can displace the ligated distal histidine to produce a ferrous CO form which has a low steady-state photolability, indicating that the replacement histidine blocks the CO escape route from the binding site.

Erythropoietin enhances vascular responsiveness to norepinephrine in renal failure. The mechanism of hypertension induced by recombinant human erythropoietin (rHuEPO) is unclear but may include an increase in peripheral vascular resistance. We studied changes of arterial pressure and plasma endothelin in nine consecutive hemodialysis patients before, and 6 and 12 weeks after, starting rHuEPO. In six patients, changes in cardiac index (CI), stroke index (SI) and total peripheral resistance index (TPRI) were measured by bioimpedance, and forearm vascular responsiveness to intra-arterial norepinephrine (30 to 240 pmol/min) and endothelin-1 (5 pmol/min) were assessed. Six healthy age and sex matched subjects also underwent assessment of forearm vascular responsiveness to norepinephrine and endothelin-1. Treatment with rHuEPO significantly increased hemoglobin and mean arterial pressure (MAP). TPRI also increased by 35 ± 11%. Plasma endothelin, although elevated basally, remained unchanged. Intra-arterial infusion of norepinephrine caused a maximal increase in forearm vascular resistance (FVR) of 17 ± 9% before rHuEPO, significantly less than the 32 ± 5% increase in healthy control subjects (P = 0.04). The response increased to 65 ± 15% (P = 0.03) after 12 weeks rHuEPO treatment (P = 0.51 vs. controls). Endothelin-1 caused a maximal increase of FVR at 60 minutes of 45 ± 24% before rHuEPO, which was not significantly different from controls, and tended to decrease with rHuEPO therapy. The response to endothelin-1, but not norepinephrine, correlated inversely with MAP (r = -0.52; P = 0.03) and TPRI (r = -0.51; P = 0.04). In conclusion, these studies show that anemia in chronic renal failure is associated with depressed vascular responsiveness to norepinephrine which is restored by rHuEPO therapy. In contrast, vascular responses to endothelin-1 tend to reduce with rHuEPO therapy. The change in vascular responsiveness to norepinephrine may contribute to the increase in arterial pressure associated with rHuEPO therapy.

The results of a longitudinal study assessing the impact of internal constraints upon both organizational responsiveness to the environment and efforts to change structures for symbolic signaling of policy are presented. The causal model used is developed from a theoretical elaboration of Williamson, Thompson, and Meyer. The implications of the analysis for the signaling metaphor of organizational change are emphasized. The data indicate (i) that the varying resistance to change observed within core dimensions of organizational structure may be largely due to durable capital investments, (ii) that within capitalized dimensions of organizational structure, the resulting resistance to change leads to a longitudinal persistence of centralized decision making, and (iii) that failure to incorporate such constraints in analyses of organizational change leads to misleading results.

In 30 patients with acute myocardial infarction complicated by either advanced atrioventricular or bundle branch block, pulmonary arterial wedge pressures were studied in relation to clinical and radiographic features of left ventricular failure, changes in central venous and pulmonary arterial pressures, and arterial hypoxemia. An increase in mean pulmonary arterial wedge pressure was poorly correlated with the presence of dyspnea, audible third or fourth heart sounds, or persistent basal rales; however, it was significantly related to radiographic evidence of pulmonary venous dilatation or edema, a systolic blood pressure of less than 100 mm Hg, gallop rhythm associated with tachycardia, and heart rate in patients with sinus rhythm and normal atrioventricular conduction. Increased mean right atrial pressure indicated increased mean pulmonary arterial wedge pressure in patients with isolated anterior infarction, but in several patients with isolated inferior infarction the level of right atrial pressure was disproportionately high. The pulmonary arterial diastolic pressure closely reflected the mean pulmonary arterial wedge pressure in the absence of obstructive airways disease or pulmonary embolism. The level of the arterial oxygen tension fell as the mean pulmonary arterial wedge pressure rose, but it was considerably reduced in some patients with only moderately increased pressures. However, the latter usually had radiographic evidence of pulmonary venous dilatation or edema, suggesting that the pressure had been elevated previously to higher levels.