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6-Methoxyquinoline (6MQ) and acridine are known to become more basic when excited to their lowest singlet state. We utilized a direct time-resolved subnanosecond technique and steady-state fluorescence to determine the acid-base kinetics of these excited compounds * + HzO <=* * + + OH" (A,, A.]). The protonation rates (A,) were found to be 5.2 X 106 M"1 s"1 and 0.2 X 106 M~* s'1 for 6MQ (p/f* = 11.8) and acridine (pK* = 10.7), respectively. The neutralization rate (A-) was found to be diffusion controlled (6MQ) A_, = 3.1 X 10 M"1 s"1. The deuterium isotope effects were found to be kf/kf = 3.5 and A_!H/A_iD = 2.2. The protonation rate increased in the presence of metal cations; for acridine in 2 M Mg(N03)2 solution k^= 73 X 106 M"1 s"*.

Cooperation among genetically unrelated individuals is commonly explained by the potential for future reciprocity or by the risk of being punished by group members. However, unconditional altruism is more difficult to explain. We demonstrate that unconditional altruism can evolve as a costly signal of individual quality (i.e. a handicap) as a consequence of reciprocal altruism. This is because the emergent correlation between altruism and individual quality in reciprocity games can facilitate the use of altruism as a quality indicator in a much wider context, outside the reciprocity game, thus affecting its further evolution through signalling benefits. Our model, based on multitype evolutionary game theory shows that, when the additive signalling benefit of donating help exceeds the cost for only some individuals (of high-quality state) but not for others (of low-quality state), the population possesses an evolutionarily stable strategy (ESS) profile wherein high-quality individuals cooperate unconditionally while low-quality individuals defect or play titfor-tat (Tf T). Hence, as predicted by Zahavi's handicap model, signalling benefits of altruistic acts can establish a stable generosity by high-quality individuals that no longer depends on the probability of future reciprocation or punishment.

Introduction The sacroiliac joint (SIJ) has been estimated to contribute to pain in as much as 38% of cases of lower back pain. There are no clear diagnostic or treatment pathways. This article seeks to establish a clearer pathway and algorithm for treating patients. Methods The literature was reviewed in order to review the biomechanics, as well as establish the various diagnostic and treatment options. Diagnostic factors addressed include etiology, history, physical exam, and imaging studies. Treatment options reviewed include conservative measures, as well as interventional and surgical options. Results Proposed criteria for diagnosis of sacroiliac joint dysfunction can include pain in the area of the sacroiliac joint, reproducible pain with provocative maneuvers, and pain relief with a local anesthetic injection into the SIJ. Conventional non-surgical therapies such as medications, physical therapy, radiofrequency denervation, and direct SI joint injections may have some limited durability in therapeutic benefit. Surgical fixation can be by a lateral or posterior/posterior oblique approach with the literature supporting minimally invasive options for improving pain and function and maintaining a low adverse event profile. Conclusion SIJ pain is felt to be an underdiagnosed and undertreated element of LBP. There is an emerging disconnect between the growing incidence of diagnosed SI pathology and underwhelming treatment efficacy of medical treatment. This has led to an increase in SI joint fixation. We have created a clearer diagnostic and treatment pathway to establish an algorithm for patients that can include conservative measures and interventional techniques once the diagnosis is identified.

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