Moral Blameworthiness and the Reactive Attitudes

In this paper, I present and defend a novel version of the Reactive Attitude account of moral blameworthiness. In Section 1, I introduce the Reactive Attitude account and outline Allan Gibbard’s version of it. In Section 2, I present the Wrong Kind of Reasons Problem, which has been at the heart of much recent discussion about the nature of value, and explain why a reformulation of it causes serious problems for versions of the Reactive Attitude account such as Gibbard’s. In Section 3, I consider some ways in which Gibbard might attempt to avoid the Wrong Kind of Reason Problem. I argue that all of these ways fail to achieve their aim and further contend that the Wrong Kind of Reason Problem cannot be solved in a sufficiently convincing manner by the widely used method of making ad hoc distinctions among kinds of properties, kinds of attitudes, and kinds of reasons. In Section 4, I sketch my own version of the Reactive Attitude account of moral blameworthiness and show that it simply avoids the Wrong Kind of Reason Problem rather than attempting to solve the problem on a piecemeal basis.     

Motion aftereffects and retinal motion

Two experiments are described in which it was investigated whether the adaptation on which motion aftereffects (MAEs) are based is a response to retinal image motion alone or to the motion signal derived from the process which combines the image motion signal with information about eye movement (corollary discharge). In both experiments observers either fixated a stationary point or tracked a vertically moving point while a pattern (in experiment 1, a grating; in experiment 2, a random-dot pattern) drifted horizontally across the field. In the tracking condition the adapting retinal motion was oblique. In the fixation condition it was horizontal. In every case in both conditions the MAE was horizontal, in the direction opposite to that of pattern motion. These results are consistent with the hypothesis that the adaptation is a response to the motion signal derived from the comparison of eye and image motion rather than to retinal motion per se. An alternative explanation is discussed.     

The effects of nicotine on Parkinson's disease

Post-mortem studies have demonstrated a substantial loss of nicotinic receptors in Parkinson's disease (PD), which may be at least partially responsible for some of the cognitive, motoric, and behavioral deficits seen in this disorder. Epidemiologic studies have suggested that cigarette smoking is a strong negative risk factor for the development of PD. We have previously shown that blockade of central nicotinic receptors produces cognitive impairment in areas of new learning, short-term memory, and psychomotor slowing with increasing dose sensitivity with age and disease. Studies of acute stimulation of nicotinic receptors in Alzheimer's disease with nicotine and the novel agonist ABT-418 in our laboratory and others have shown improvements in several measures of cognitive function. Prior studies of the effects of nicotine in PD have suggested some improvements in clinical symptomatology. We have begun quantitative studies of both acute and chronic nicotine in PD to assess both cognitive and motor effects. Fifteen (15) nondemented subjects (age 66 +/- 5.3; M/F = 11/4) with early to moderate PD (mean Hoehn-Yahr stage = 1.77; MMSE = 28.6) received a dose-ranging study of intravenous nicotine up to 1.25 microg/kg/min, followed by chronic administration of nicotine by transdermal patch with doses ranging up to 14 mg per day for 2 weeks. Testing occurred both during drug administration and up to 2 months after drug cessation to look for prolonged effects. Preliminary analysis shows improvements after acute nicotine in several areas of cognitive performance, particularly measures such as reaction time, central processing speed, and decreased tracking error. Improvements in attention and semantic retrieval were not seen. After chronic nicotine, improvements were seen in several motor measures suggesting improved extrapyramidal functioning. This appeared to be sustained for up to 1 month after drug. The treatment was well tolerated. Nicotinic stimulation may have promise for improving both cognitive and motor aspects of Parkinson's disease.     

Race, pharmacogenomics, and marketing: putting BiDil in context

This article endeavors to place into context recent developments surrounding the United States Food and Drug Administration recent approval of BiDil (isosorbide dinitrate/hydralazine hydrochloride) (NitroMed, Inc., Lexington, MA) as the first ever race-specific drug--in this case to treat heart failure in African Americans. It focuses in particular on both commercial incentives and statistical manipulation of medical data as framing the drive to bring BiDil to market as a race-specific drug. In current discourse about pharmacogenomics, targeting a racial audience is perceived as necessary because at this point the technology and resources do not exist to scan efficiently every individual's genetic profile. The article argues that medical researchers may say they are using race as a surrogate to target biology in drug development, but corporations are using biology as a surrogate to target race in drug marketing. Pharmacogenomics may hold great promise, but on our way to that Promised Land, it is imperative to review such short cuts with a critical eye.