Meaning, soul, state of mind, and hope.
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Argument about the ethical possibility of the therapeutic use of embryonic stem cells depends critically on the evaluation of the moral status of the very early embryo. Some assert that at the blastocyst stage it is only potentially human, not yet possessing the full ethical status of personhood, while others assert that from its formation the embryo possesses all the moral rights of a human person. It is shown that a decision on this issue is closely related to how human nature is to be understood. The idea of a person as a dual combination of body and spirit correlates naturally with the assertion of absolute personhood from conception, while an idea of human psychosomatic unity encourages a development picture in which the embryo only grows gradually into personhood. The latter view is seen to be encouraged by new advances in science which emphasise the importance of the concept of information in the discussion of complex systems. Other ethical issues related to human genetics are also briefly reviewed.
Ken Himma argues that a human being becomes a moral person at the commencement of brain activity. In response to Himma, the author offers (1) brief comments on Himma's project, (2) an alternative account of the human person that maintains that a human being is a human person by nature as long as it exists, and (3) a counterexample to Himma's position that shows it cannot account for the wrongness of the purposeful creation of anencephalic-like children. The author concludes with replies to two challenges to his position.
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BACKGROUND: In patients with symptoms of heart failure, elevations in B-type natriuretic peptide (BNP) accurately identify ventricular dysfunction. However, BNP levels are not specific for ventricular dysfunction in patients who do not have overt symptoms of heart failure, suggesting that other cardiac processes such as myocardial ischemia may also cause elevations in BNP. METHODS AND RESULTS: To determine whether BNP elevations are associated with myocardial ischemia, we measured plasma BNP levels before performing exercise treadmill testing with stress echocardiography in outpatients with stable coronary disease. Of the 355 participants, 113 (32%) had inducible ischemia. Compared with participants in the lowest BNP quartile (0 to 16.4 pg/mL), those in the highest quartile of BNP (> or =105 pg/mL) had double the risk of inducible ischemia (adjusted relative risk, 2.0; 95% CI, 1.2 to 2.6; P=0.008). The relation between elevated BNP levels and inducible ischemia was especially evident in the 206 participants who had a history of myocardial infarction (adjusted relative risk, 2.6; 95% CI, 1.5 to 3.7, P=0.002) and was absent in those without a history of myocardial infarction (adjusted relative risk, 1.0; 95% CI, 0.3 to 2.2; P=0.9). This association between BNP levels and inducible ischemia remained strong after adjustment for measures of systolic and diastolic dysfunction. CONCLUSIONS: Elevated levels of BNP are independently associated with inducible ischemia among outpatients with stable coronary disease, particularly among those with a history of myocardial infarction. The observed association between BNP levels and ischemia may explain why tests for BNP are not specific for ventricular dysfunction among patients with coronary disease.
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BACKGROUND: Fetuin-A is a multifunctional hepatic secretory protein that inhibits the action of insulin in experimental animals. We evaluated the association between human serum fetuin-A and the metabolic syndrome (MetS) in a cohort of persons with coronary artery disease. METHODS AND RESULTS: We defined MetS by the National Cholesterol Education Program criteria among 711 nondiabetic outpatients with coronary artery disease. The mean age was 67 years, and 82% were male. We divided participants into quartiles by serum fetuin-A concentrations. A total of 45% of participants (80 of 177) in the highest quartile of fetuin-A had MetS compared with 24% of participants (42 of 177) in the lowest quartile (odds ratio, 2.7; 95% confidence interval, 1.7 to 4.2; P<0.001). This association persisted after adjustment for potential confounding variables, including hypertension, body mass index, and inflammatory biomarkers (adjusted odds ratio, 2.0; 95% confidence interval, 1.1 to 3.5; P=0.02). Higher fetuin-A quartiles were also strongly and independently associated with higher low-density lipoprotein, non-high-density lipoprotein (HDL), and triglyceride concentrations and lower HDL concentrations (all P<0.01). CONCLUSIONS: Higher human fetuin-A concentrations are strongly associated with MetS and an atherogenic lipid profile. Future studies should evaluate whether fetuin-A predicts coronary artery disease risk.
BACKGROUND: Serum creatinine and related estimating equations predict cardiovascular events and mortality among persons with coronary heart disease (CHD). Cystatin C is a novel and sensitive endogenous marker of kidney function. Whether cystatin C concentrations are associated with adverse events among ambulatory persons with CHD is unknown. METHODS AND RESULTS: Nine hundred ninety ambulatory persons with CHD were categorized into quartiles of serum cystatin C at inception, with < or = 0.91 mg/L constituting the lowest quartile (I) and > or = 1.30 mg/L constituting the highest (IV). Cox proportional hazards models evaluated time to all-cause mortality, cardiovascular events (composite of CHD death, myocardial infarction, and stroke), and incident heart failure. After a median follow-up of 37 months, 132 participants (13%) died, 101 (10%) had cardiovascular events, and 57 (7%) had incident heart failure. Compared with participants in the lowest cystatin C quartile, those in the highest quartile were at increased risk of all-cause mortality (hazard ratio, 3.6; 95% CI, 1.8 to 7.0), cardiovascular events (hazard ratio, 2.0; 95% CI, 1.0 to 3.8), and incident heart failure (hazard ratio, 2.6; 95% CI, 1.0 to 6.9) in analyses adjusted for traditional cardiovascular risk factors. Cystatin C in the highest quartile predicted similar risk for these outcomes among participants with lower (< or = 60 mL/min per 1.73 m2) or higher estimated glomerular filtration rate and among participants with or without microalbuminuria. CONCLUSIONS: High cystatin C concentrations predict substantial increased risks of all-cause mortality, cardiovascular events, and incident heart failure among ambulatory persons with CHD. This risk is not completely captured by measures of kidney function routinely used in clinical practice.
This study tested the hypothesis that Williams syndrome, a rare genetic neurodevelopmental disorder with an unusual cognitive phenotype, involves spared abilities in the domain of understanding other minds. A group of retarded adults with Williams syndrome was compared to an age-, IQ-, and language-matched group of adults with Prader-Willi syndrome, another genetic disorder without the cognitive characteristics of Williams syndrome, and a group of age-matched normal adults, on a task that taps mentalizing ability. The task involved selecting the correct labels to match photographs of complex mental state expressions in the eye region of the face. The adults with Williams syndrome performed significantly better than the adults with Prader-Willi on this task, and about half the group performed in the same range as the normal adults. These findings are consistent with anecdotal evidence about Williams syndrome and provide evidence that mentalizing is a distinct cognitive domain. This spared cognitive capacity may be linked to the relative sparing of limbic-cerebellar neural substrate in Williams syndrome, which is also connected to cortico-frontal regions that are known to be involved in understanding complex mental states.
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OBJECTIVE: Depressive symptoms are associated with an increased risk of cardiac events in patients with heart disease. Elevated catecholamine levels may contribute to this association, but whether depressive symptoms are associated with catecholamine levels in patients with heart disease is unknown. METHOD: The authors examined the association between depressive symptoms (defined by a Patient Health Questionnaire score > or =10) and 24-hour urinary norepinephrine, epinephrine, and dopamine excretion levels in 598 subjects with coronary disease. RESULTS: A total of 106 participants (18%) had depressive symptoms. Participants with depressive symptoms had greater mean norepinephrine excretion levels than those without depressive symptoms (65 microg/day versus 59 mug/day, with adjustment for age, sex, body mass index, smoking, urinary creatinine levels, comorbid illnesses, medication use, and cardiac function). In logistic regression analyses, participants with depressive symptoms were more likely than those without depressive symptoms to have norepinephrine excretion levels in the highest quartile and above the normal range. Depressive symptoms were not associated with dopamine or epinephrine excretion levels. CONCLUSIONS: In patients with coronary disease, depressive symptoms are associated with elevated norepinephrine excretion levels. Future longitudinal studies are needed to determine whether elevations in norepinephrine contribute to adverse cardiac outcomes in patients with depressive symptoms.
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