Resonant Activation of Population Extinctions

Understanding the mechanisms governing population extinctions is of key importance to many problems in ecology and evolution. Stochastic factors are known to play a central role in extinction, but the interactions between a population's demographic stochasticity and environmental noise remain poorly understood. Here, we model environmental forcing as a stochastic fluctuation between two states, one with a higher death rate than the other. We find that in general there exists a rate of fluctuations that minimizes the mean time to extinction, a phenomenon previously dubbed "resonant activation." We develop a heuristic description of the phenomenon, together with a criterion for the existence of resonant activation. Specifically the minimum extinction time arises as a result of the system approaching a scenario wherein the severity of rare events is balanced by the time interval between them. We discuss our findings within the context of more general forms of environmental noise, and suggest potential applications to evolutionary models.Comment: 12 pages, 7 Figures, Accepted for publication in Physical Review

Effect of continuous gamma-ray exposure on performance of learned tasks and effect of subsequent fractionated exposures on blood-forming tissue

Sixteen monkeys trained to perform continuous and discrete-avoidance and fixed-ratio tasks with visual and auditory cues were performance-tested before, during, and after 10-day gamma-ray exposures totaling 0, 500, 750, and 1000 rads. Approximately 14 months after the performance-test exposures, surviving animals were exposed to 100-rad gamma-ray fractions at 56-day intervals to observe injury and recovery patterns of blood-forming tissues. The fixed-ratio, food-reward task performance showed a transient decline in all dose groups within 24 hours of the start of gamma-ray exposure, followed by recovery to normal food-consumption levels within 48 to 72 hours. Avoidance tasks were performed successfully by all groups during the 10-day exposure, but reaction times of the two higher dose-rate groups in which animals received 3 and 4 rads per hour or total doses of 750 and 1000 rads, respectively, were somewhat slower

The structure of triphenylgermanium hydroxide

C18H~6GeO, Mr = 320.9, triclinic, Pi, a = 15.408 (6), b = 19.974 (7), c = 23.264 (11) A, a = 107.78 (4), 13 = 1.03.54 (4), y= 101.51 (3) °, V = 6338 (5)/~3, Z = 16, Dx = 1.34 g cm -3, a(Mo Ka) = 0.71073A, /z = 19.1cm-1, F(000)=2624, T= 293 K, R = 0.055 for 6846 observed reflections. The eight independent molecules in the asymmetric unit form two independent O--H...O hydrogen-bonded tetramers with the O atoms in a flattened tetrahedral arrangement [hydrogen-bond distances in the range 2.609 (11) to 2.657 (11)A]. The Ge atoms are tetrahedrally coordinated with mean Gc O 1.791 (7) and Gc C 1.931 (8) A

Twisted [(R3P)PdX] groups above dicarbaborane ligands: 4-dimethylsulfido-3-iodo-3-triphenylphosphine-closo-3-pallada-1,2-dicarbadodecaborane and 3-dimethylphenylphosphine-3-chloro-4-dimethylsulfido-closo-3-pallada-1,2-dicarbadodecaborane

The structural analyses of [3-(PPh₃)-3-I-4-(SMe₂)-closo-3,1,2-PdC₂B₉H₁₀] or [Pd(C₄H₁₆B₉S)I(C₁₈H₁₅P)], (I), and [3-(PPhMe₂)-3-Cl-4-(SMe₂)-closo-3,1,2-PdC₂B₉H₁₀] or [Pd(C₄H₁₆B₉S)Cl(C₈H₁₁P)], (II), show that in comparison with [3-(PR₃)2-closo-3,1,2-PdC₂B₉H₁₁] the presence of the 4-SMe₂ group causes the [PdX(PR₃)] unit (X = halogen) to twist about an axis passing through the Pd atom and the directly opposite B atom of the carbaborane ligand. The halogen atoms are located almost directly above a C atom in the C₂B₃ face, and the conformations of the [PdX(PR₃)] units above the C₂B₃ faces are not those predicted from molecular orbital calculations of the closo-3,1,2-PdC₂B₉ system. The fact that the variation from the predicted conformation is greater in the case of (I) than in (II) may be ascribed to the greater steric interactions induced by the I atom in (I) compared with the Cl atom in (II)