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This paper treats a general equilibrium existence problem on overlapping generations (OLG) economies with satiated agents and fiat money. The setting is important because it allows the analysis to incorporate Pareto optimality problems of the type where the value functions do not necessarily converge. For example, this is the case for optimal allocations such as a basic income under a budget deficit, which can only be realized with policies that require non-negative wealth transfers for all agents. Because of the existence of satiated agents, our argument can be identified with a dividend equilibrium (Aumann and Dreze 1986) or an equilibrium with slack (Mas-Colell 1992). For OLG settings, however, some conditions (like arguments for strictly positive endowments, resource relatedness and minimum wealth conditions with negative prices, and limit arguments for dividends) must be reconsidered. We note that by considering the OLG framework together with satiated agents, not only can the existence of a monetary equilibrium be assumed in advance, but the existence of a monetary equilibrium based on an arbitrary money supply is guaranteed. Taking into account that our setting includes production (without discount factor), the model here provides a basis for a wide range of difficult problems, including the player’s (equilibrium-dependent) survival problem, multi-sectoral capital accumulation, bequests, firm formation, and so on.

Masatake Kurita,1–3 Takahiro Moriya,2 Satoshi Nishino,2,4 Eishin Hirata,4 Noriyasu Hirasawa,5 Yoshiro Okubo,3 Tadahiro Sato4 1Wakamiya Hospital, Koutokukai, Yoshihara, Yamagata, 2Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, 3Department of Psychiatry and Behavioral Science, Graduate School of Medicine, Nippon Medical School, Sendagi, Tokyo, 4Sato Hospital, Koutokukai, Kunugizuka, Nanyo, Yamagata, 5Laboratory of Pharmacotherapy of Life-Style Related Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan Abstract: A woman was diagnosed with non-24-hour sleep–wake syndrome and depressive symptoms. Her depressive symptoms did not respond to standard doses of several antidepressants or mood stabilizers. Furthermore, her sleep–wake cycle remained non-entrained despite treatment with a melatonin-related drug, vitamin B12, and phototherapy. Ultimately, her sleep–wake rhythm was restored to a 24-hour pattern with a low dose of valproic acid, and her depressive symptoms tended to improve as a result of synchronization without antidepressants. Low-dose valproic acid appears to be one of the effective means of entraining circadian rhythms in patients with non-24-hour sleep–wake syndrome, which in turn likely improves associated depressive symptoms. Keywords: circadian rhythm sleep disorder, mood stabilizers, vitamin B12, melatonin, phototherapy, antidepressants,depression

Daily rhythms such as sleep-wake, feeding, and the core body temperature, persist with a period of approximately 24 hr even in the absence of environmental time cues, suggesting the existence of an endogenous time-keeping system, the circadian clock. In mammals, the circadian clock is located in the suprachiasmatic nucleus of the hypothalamus (SCN). Recently, a number of studies have revealed that circadian oscillations in the SCN are driven by the intracellular transcriptional and post-translational negative feedback loop formed by several clock-related genes such as Period (Per) and clock genes. Surprisingly, this feedback loop was found in many peripheral organs, indicating that the physiological and pathological rhythms in the peripheral organs were generated by the local clock in the peripheral organs, which synchronize to the central clock in the SCN. In addition several humoral factors seem to medi- aa, ate communication between the central and peripheral clocks. Furthermore, the transcription of some genes encoding the disease risk factors were found to be directly regulated by the clock genes, suggesting the possible involvement of clock genes in the onset of some diseases. In this article, we review the current view on the molecular mechanism underlying circadian oscillations in the central clock within the SCN and the local clock in the peripheral and discuss the relationship between clock genes, and physiological and pathological rhythm., Acta medica Nagasakiensia. 2003, 48(1-2), p.1-7

1. The mPer1 and mPer2 genes are putative mouse clock genes that regulate circadian oscillator present in the suprachiasmatic nucleus (SCN) neuron. While they are also expressed in the granular cell layer in the cerebellum, their function is unknown. In a first step to verify the physiological roles of mPer1 and mPer2 genes in the cerebellum, we examined the effects of benzodiazepines on the expression of the mPer1 and mPer2 genes. 2. mPer2 mRNA expression was higher at ZT16 than ZT4 in the mouse cerebellum. 3. High-dose administration of diazepam (10 mg kg-1) or triazolam (1 mg kg-1) reduced mPer1 mRNA level 1 h after treatment in the cerebellum. 4. Reduced expression of mPer1 by diazepam treatment was transient. No difference of mPer1 mRNA level between diazepam (10 mg kg-1)- and vehicle-treated group was observed 6 h after treatment. 5. Administration of high doses of tandospirone (30 mg kg-1), a non-benzodiazepine anxiolytic also reduced mPer1 mRNA expression 1 h after treatment. 6. Administration of high doses of clozapine (5 mg kg-1) or haloperidol (1 mg kg-1) impaired the rota-rod performance without affecting on mPer1 mRNA level. 7. Diazepam and tandospirone inhibited the expression of mPer1 mRNA in the primary cultured cerebellum granule cells. 8. Transient reductions of mPer1 mRNA levels by various benzodiazepines and tandospirone is associated with impairment of coordinated movement, such as rota-rod performance and equilibrium.