Limit cycles for cubic systems with a symmetry of order 4 and without in nite critical points

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Limit Cycles for a class of three dimensional polynomial differential systems

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On the upper bound of the number of limit cycles obtained by the second order averaging method I

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On the upper bound of the number of limit cycles obtained by the second order averaging method II

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Geometric tools to determine the hyperbolicity of limit cycles

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Multiplicity of limit cycles and analytic m-solutions for planar differential systems

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On the existence and uniqueness of limit cycles in Liénard differential equations allowing discontinuities

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Characterization of larval moulting cycles in Maja brachydactyla (Brachyura, Majidae) reared in the laboratory

The moulting cycles of all larval instars (zoea I, zoea II, and megalopa) of the spider crab Maja brachydactyla Balss 1922 were studied in laboratory rearing experiments. Morphological changes in the epidermis and cuticle were photographically documented in daily intervals and assigned to successive stages of the moulting cycle (based on Drach's classification system). Our moult-stage characterizations are based on microscopical examination of integumental modifications mainly in the telson, using epidermal condensation, the degree of epidermal retraction (apolysis), and morphogenesis (mainly setagenesis) as criteria. In the zoea II and megalopa, the formation of new setae was also observed in larval appendages including the antenna, maxillule, maxilla, second maxilliped, pleopods, and uropods. As principal stages within the zoea I moulting cycle, we describe postmoult (Drach's stages A–B combined), intermoult (C), and premoult (D), the latter with three substages (D0, D1, and D2). In the zoea II and megalopa, D0 and D1 had to be combined, because morphogenesis (the main characteristic of D1) was unclear in the telson and did not occur synchronically in different appendices. The knowledge of the course and time scale of successive moult-cycle events can be used as a tool for the evaluation of the developmental state within individual larval instars, providing a morphological reference system for physiological and biochemical studies related to crab aquaculture.

Boundedly rational credit cycles

We propose an evolutionary model of a credit market. We show that theeconomy exhibits credit cycles. The model predicts dynamics which are consistent with some evidence about the Great Depression. Real shocks triggerepisodes of credit--crunch which are observed in the process of adjustmenttowards the post shock equilibrium.

Is lumpy investment really irrelevant for the business cycle?

New-Keynesian (NK) models can only account for the dynamic effects of monetary policy shocks if it is assumed that aggregate capital accumulation is much smoother than it would be the case under frictionless firm-level investment, as discussed in Woodford (2003, Ch. 5). We find that lumpy investment, when combined with price stickiness and market power of firms,can rationalize this assumption. Our main result is in stark contrast with the conclusions obtained by Thomas (2002) in the context of a real business cycle (RBC) model. We use our model to explain the economic mechanism behind this difference in the predictions of RBC and NK theory.

Sources and propagation of international cycles: Common shocks or transmission?

This paper studies the generation and transmission of international cycles in a multi-country model with production and consumption interdependencies. Two sources of disturbance are considered and three channels of propagation are compared. In the short run the contemporaneous correlation of disturbances determines the main features of the transmission. In the medium run production interdependencies account for the transmission of technology shocks and consumption interdependencies account for the transmission of government shocks. Technology disturbances, which are mildly correlated across countries, are more successful than government expenditure disturbances in reproducing actual data. The model also accounts for the low cross country consumption correlations observed in the data.

Lobbying, innovation and protectionist cycles

This paper explains why trade liberalizations occur in developing countries,and why they are often reversed. It does so by focusing on the use oflobbying for protection by import competing firms as a means to postponecostly product quality upgrades to keep up with foreign competitors. Giventhe availability of a political market for import tariffs, domestic firmswill lobby for a sequence of tariffs that insulate domestic profits from awidening quality gap, thereby allowing adjustment to be postponed. But asthe contributions required by the government grow with the size of thequality gap, it will be optimal to adjust quality and to decrease thelobbying effort at some time, leading to liberalization and technologicalcatch-up. But then the equilibrium tariff will again be small and "cheap",and it will pay to start lobbying anew, until the next quality adjustment.Therefore, cycles in protection will occur as a result of the use oflobbying as a substitute for innovation. The model thus sheds new light onthe impact of the costs of protection on the effectiveness of the lobbyingeffort over time, and on their implications for the timing and the timehorizon of trade reforms in developing countries.

Irreversible investment in stochastically cyclical markets

This paper presents a new framework for studying irreversible (dis)investment whena market follows a random number of random-length cycles (such as a high-tech productmarket). It is assumed that a firm facing such market evolution is always unsure aboutwhether the current cycle is the last one, although it can update its beliefs about theprobability of facing a permanent decline by observing that no further growth phasearrives. We show that the existence of regime shifts in fluctuating markets suffices for anoption value of waiting to (dis)invest to arise, and we provide a marginal interpretationof the optimal (dis)investment policies, absent in the real options literature. Thepaper also shows that, despite the stochastic process of the underlying variable has acontinuous sample path, the discreteness in the regime changes implies that the samplepath of the firm s value experiences jumps whenever the regime switches all of a sudden,irrespective of whether the firm is active or not.

The Brauer group and the second Abel-Jacobi map for 0-cycles on algebraic varieties

This paper focuses on the connection between the Brauer group and the 0-cycles of an algebraic variety. We give an alternative construction of the second l-adic Abel-Jacobi map for such cycles, linked to the algebraic geometry of Severi-Brauer varieties on X. This allows us then to relate this Abel-Jacobi map to the standard pairing between 0-cycles and Brauer groups (see [M], [L]), completing results from [M] in this direction. Second, for surfaces, it allows us to present this map according to the more geometrical approach devised by M. Green in the framework of (arithmetic) mixed Hodge structures (see [G]). Needless to say, this paper owes much to the work of U. Jannsen and, especially, to his recently published older letter [J4] to B. Gross.

Gp74 a membrane glycoprotein of the cis-Golgi network that cycles through the endoplasmic reticulum and intermediate compartment

A monoclonal antibody CC92 (IgM), raised against a fraction of rat liver enriched in Golgi membranes, recognizes a novel Endo H-resistant 74-kD membrane glycoprotein (gp74). The bulk of gp74 is confined to the cis-Golgi network (CGN). Outside the Golgi gp74 is found in tubulovesicular structures and ER foci. In cells incubated at 37 degrees C the majority of gp74 is segregated from the intermediate compartment (IC) marker p58. However, in cells treated with organelle perturbants such as low temperature, BFA, and [AIF4]- the patterns of the two proteins become indistinguishable. Both proteins are retained in the Golgi complex at 20 degrees C and in the IC at 15 degrees C. Incubation of cells with BFA results in relocation of gp74 to p58 positive IC elements. [AIF4]- induces the redistribution of gp74 from the Golgi to p58-positive vesicles and does not retard the translocation of gp74 to IC elements in cells treated with BFA. Disruption of microtubules by nocodazol results in the rapid disappearance of the Golgi elements stained by gp74 and redistribution of the protein into vesicle-like structures. The responses of gp74 to cell perturbants are in sharp contrast with those of cis/middle and trans-Golgi resident proteins whose location is not affected by low temperatures or [AIF4]-, are translocated to the ER upon addition of BFA, and stay in slow disintegrating Golgi elements in cells treated with nocodazol. The results suggest that gp74 is an itinerant protein that resides most of the time in the CGN and cycles through the ER/IC following the pathway used by p58.