We use data on police-involved deaths to estimate how the risk of being killed by police use of force in the United States varies across social groups. We estimate the lifetime and age-specific risks of being killed by police by race and sex. We also provide estimates of the proportion of all deaths accounted for by police use of force. We find that African American men and women, American Indian/Alaska Native men and women, and Latino men face higher lifetime risk of being killed by police than do their white peers. We find that Latina women and Asian/Pacific Islander men and women face lower risk of being killed by police than do their white peers. Risk is highest for black men, who (at current levels of risk) face about a 1 in 1,000 chance of being killed by police over the life course. The average lifetime odds of being killed by police are about 1 in 2,000 for men and about 1 in 33,000 for women. Risk peaks between the ages of 20 y and 35 y for all groups. For young men of color, police use of force is among the leading causes of death.

Many gastrointestinal muscles generate rhythmic contractions that are associated with slow waves (Tomita, 1981;Sanders, 1992). Several observations suggest that activity originates in interstitial cells of Cajal (ICC), and that smooth muscle cells act as follower cells (Sanders, 1996). Thus, when regions containing ICC are cut away, slow waves are abolished (Smith et al. 1987). Similarly intestinal preparations obtained from strains of mice which lack ICC, fail to generate normal slow waves (Ward et al. 1994;Huizinga et al. 1995). In guinea-pig antrum, ICC generate large amplitude driving potentials which depolarize the circular layer. The depolarization triggers a secondary regenerative response, so giving rise to a complete slow wave (Dickens et al. 1999). Previous analyses of slow waves have suggested that they resulted from the sequential activation of voltage-dependent ion channels (Sanders, 1992). However, when single bundles of circular muscle from the antral region of guinea-pig stomach were stimulated directly, they generated regenerative potentials that did not depend upon the activation of conventional voltage-dependent ion channels. Rather they appeared to involve the voltage-activated release of internal Ca¥ following the production of a second messenger like inositol trisphosphate . Membrane depolarizations, that do not involve conventional voltage-dependent ion channels, are generated when increases in [Ca¥]é activate ion selective channels that allow an accumulation of internal positive charge (van Helden,

Slow waves were recorded from the circular muscle layer of the antral region of guinea‐pig stomach. Slow waves were abolished by 2APB, an inhibitor of IP3‐induced Ca2+ release. When the rate of generation of slow waves was monitored it was found to vary from cycle to cycle around a mean value. The variation persisted after abolishing neuronal activity with tetrodotoxin. When simultaneous recordings were made from interstitial cells in the myenteric region (ICCMY) and smooth muscle cells of the circular layer, variations in the rate of generation of slow waves were found to be linked with variations in the rate of generation of driving potentials by ICCMY. A preparation was devised which consisted of the longitudinal muscle layer and ICCMY. In this preparation ICCMY and smooth muscle cells lying in the longitudinal muscle layer generated driving potentials and follower potentials, synchronously. Driving potentials had two components, a rapid primary component that was followed by a prolonged plateau component. Caffeine (3 mM) abolished the plateau component; conversely reducing the external concentration of calcium ions [Ca2+]o mainly affected the primary component. Analysis of the variations in the rate of generation of driving potentials indicated that this arose because both the duration of individual driving potentials and the interval between successive driving potentials varied. It is suggested that the initiation of pacemaker activity in a network of ICCMY is a stochastic process, with the probability of initiating a driving potential slowly increasing, after a delay, from a low to a higher value following the previous driving potential.

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1. Current clamp studies using two patch electrodes and morphological observations have been performed in guinea-pig mesenteric arterioles to evaluate intercellular electrical couplings.2. In electron micrographs, preparations were found to have a single layer of smooth muscle cells. Typical gap junctions were readily observed between endothelial cells only.3. While immunoreactivity to connexin 40 was strongly expressed on the membranes of endothelial cells only, that to connexin 43 was expressed on both smooth muscle and endothelial cell membranes.4. Neurobiotin injected into a smooth muscle cell diffused into several neighbouring smooth muscle cells while that injected into an endothelial cell diffused into many endothelial cells.5. Acetylcholine-induced hyperpolarizations were conducted from endothelial cells to smooth muscle cells with a relative amplitude of 80.1 %. Ba 2+-induced action potentials were conducted in the opposite direction with a relative amplitude of 92.4 %.6. An electrotonic potential produced in a smooth muscle cell by current injection diminished steeply with distance as it spread along the muscle layer, plateauing at distances beyond 25 µm. An electrotonic potential produced in an endothelial cell spread within the intima with virtually no reduction. Electrotonic potentials could conduct through myoendothelial couplings, which seemed to behave as ohmic resistors without rectification.7. The coupling resistance between adjacent smooth muscle cells was estimated to be at least 90 MΩ and that between a smooth muscle cell and the whole endothelial layer to be 0.9 GΩ.8. The results indicate that although the resistance of myoendothelial couplings is appreciable, the endothelium may be important as a low resistance path connecting many smooth muscle cells.

Intracellular recordings were made from isolated bundles of the circular muscle layer of mouse gastric antrum and the responses evoked by stimulating intrinsic nerve fibres were examined. Transmural nerve stimulation evoked a fast inhibitory junction potential (fast‐IJP) which was followed initially by a smaller amplitude long lasting inhibitory junction potential (slow‐IJP) and a period of excitation. The excitatory component of the response was abolished by atropine, suggesting that it resulted from the release of acetylcholine and activation of muscarinic receptors. Fast‐IJPs were selectively reduced in amplitude by apamin and slow‐IJPs were abolished by Nω‐nitro‐l‐arginine. Slow‐IJPs were associated with a drop in membrane noise, suggesting that inhibition resulted from a reduced discharge of unitary potentials by intramuscular interstitial cells of Cajal (ICCIM). The chloride channel blocker, anthracene‐9‐carboxylic acid, reduced the discharge of membrane noise in a manner similar to that detected during the slow‐IJP. When recordings were made from the antrum of W/WV mice, which lack ICCIM, the cholinergic and nitrergic components were absent, with only fast‐IJPs being detected. The observations suggest that neurally released nitric oxide selectively targets ICCIM causing a hyperpolarization by suppressing the discharge of unitary potentials.

2. In wild-type mice interstitial cells were found at the level of the myenteric plexus (ICC MY ) and distributed within the smooth muscle bundles (ICC IM ). In these preparations slow waves, which consisted of initial and secondary components, were detected.3. In W/W V mutant mice ICC MY could be identified at the level of the myenteric plexus but ICC IM were not detected within smooth muscle bundles. Intracellular recordings revealed that smooth muscle cells generated waves of depolarization; these lacked a secondary component. These results indicate that the secondary regenerative component of a slow wave is generatedby ICC IM . Thus the depolarization arising from the pacemaker cells, ICC MY , is augmented by ICC IM , so causing a substantial membrane depolarization in the circular muscle layer. Rather than contributing directly to rhythmical electrical activity, smooth muscle cells appear to depolarize at the command of the two subpopulations of ICC.

Intracellular recordings were made from short segments of the muscular wall of the guinea-pig gastric antrum. Preparations were impaled using two independent microelectrodes, one positioned in the circular layer and the other either in the longitudinal layer, in the network of myenteric interstitial cells of Cajal (ICC MY ) or in the circular layer. Cells in each layer displayed characteristic patterns of rhythmical activity, with the largest signals being generated by ICC MY . Current pulses injected into the circular muscle layer produced electrotonic potentials in each cell layer, indicating that the layers are electrically interconnected. The amplitudes of these electrotonic potentials were largest in the circular layer and smallest in the longitudinal layer. An analysis of electrical coupling between the three layers suggests that although the cells in each layer are well coupled to neighbouring cells, the coupling between either muscle layer and the network of ICC MY is relatively poor. The electrical connections between ICC MY and the circular layer did not rectify. In parallel immunohistochemical studies, the distribution of the connexins Cx40, Cx43 and Cx45 within the antral wall was determined. Only Cx43 was detected; it was widely distributed on ICC MY and throughout the circular smooth muscle layer, being concentrated around ICC IM , but was less abundant in the circular muscle layer immediately adjacent to ICC MY . Although the electrophysiological studies indicate that smooth muscle cells in the longitudinal muscle layer are electrically coupled to each other, none of the connexins examined were detected in this layer.