Humean dispositionalism

Humean metaphysics is characterized by a rejection of necessary connections between distinct existences. Dispositionalists claim that there are basic causal powers. The existence of such properties is widely held to be incompatible with the Humean rejection of necessary connections. In this paper I present a novel theory of causal powers that vindicates the dispositionalist claim that causal powers are basic, without embracing brute necessary connections. The key assumptions of the theory are that there are natural types of causal processes, and that manifestations of powers are identified with certain kinds of causal processes. From these assumptions, the modal features of powers are explained in terms of internal relations between powers themselves and the process-types in which powers are manifested.     

Relevant Restricted Quantification

The paper reviews a number of approaches for handling restricted quantification in relevant logic, and proposes a novel one. This proceeds by introducing a novel kind of enthymematic conditional.     

Neuroprotection and the ischemic cascade

Brain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the "ischemic cascade") that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted. Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clinical and laboratory reports. In addition, a wide variety of agents have been shown to reduce infarct volume in animal models. Pharmacologic interventions that involve thrombolysis, calcium channel blockade, and cell membrane receptor antagonism have been studied and have been found to be beneficial in animal cortical stroke models. Human trials of neuroprotective therapies have been disappointing. Other than thrombolytics, no agents have shown an unequivocal benefit. The future of neuroprotection will require a logical extension of what has been learned in the laboratory and previous human trials. A sensible approach to the use of multiple-agent cocktails used in combination with thrombolytics is likely to offer the highest chance for benefit.