The exchange rate and purchasing power parity: extending the theory and tests.

This paper analyzes the exchange rate in a ``no-arbitrage' or ``real business cycle' equilibrium model and provides empirical evidence for this model vis-a-vis PPP. Our contribution is to show, based on a generalization of the equilibrium model of exchange rates, that (i) the test equation linking the exchange rate to fundamentals should allow for international heterogeneity in time preferences or risk attitudes, as well as noise---that is, the model should not be tested as an exact relation; (ii) empirical work should use levels of variables rather than first differences; (iii) tests on the existence of long-run relations should be complemented by tests on the signs of the coefficients; (iv) the specification of the regression should offer demonstrated advantages over alternatives, and the significance tests should not rely on asymptotic distributions; and (v) the tests should steer clear of countries that have imposed, for most of the period, capital restrictions or exchange controls, thus violating the integrated-markets assumption of the model. Our empirical work shows that, as a long-run relation, the generalized model outperforms PPP.Purchasing; Purchasing power; Theory; Equilibrium; Model; International; Risk; Variables; Advantages; Distribution;

The equilibrium approach to exchange rates: theory and tests.

We characterize the equilibrium exchange rate in a general equilibrium economy without imposing strong restrictions on the output processes, preferences, or commodity market imperfections. The nomial exchange rate is determined by differences in initial wealths - the currencies of richer countries tend to be overvalued, by PPP standards - and by differences of marginal indirect utilities of total nominal spending. Changes in the exchange rate mirror differences in growth rates of real spending weighted by relative risk-aversion (which can be time-varying and can differ across countries), and, in the case of non-homothetic utility functions, differences in inflation rates computed from marginal spending weights. Thus, standard regression or cointegration tests of PPP suffer from missing-variables biases and ignore variations in risk aversions across countries and over time. We also present cointegration test of the homothecy/ CRRA version of the model. When nominal spending is given an independent role (next to prices) in the short-term dynamics, both PPP and the CRRA model become acceptable.Equilibrium; Theory; Trade;

Nonmonotonic dependence of the absolute entropy on temperature in supercooled Stillinger-Weber silicon

Using a recently developed thermodynamic integration method, we compute the precise values of the excess Gibbs free energy (G^e) of the high density liquid (HDL) phase with respect to the crystalline phase at different temperatures (T) in the supercooled region of the Stillinger-Weber (SW) silicon [F. H. Stillinger and T. A. Weber, Phys. Rev. B. 32, 5262 (1985)]. Based on the slope of G^e with respect to T, we find that the absolute entropy of the HDL phase increases as its enthalpy changes from the equilibrium value at T \ge 1065 K to the value corresponding to a non-equilibrium state at 1060 K. We find that the volume distribution in the equilibrium HDL phases become progressively broader as the temperature is reduced to 1060 K, exhibiting van-der-Waals (VDW) loop in the pressure-volume curves. Our results provides insight into the thermodynamic cause of the transition from the HDL phase to the low density phases in SW silicon, observed in earlier studies near 1060 K at zero pressure.Comment: This version is accepted for publication in Journal of Statistical Physics (11 figures, 1 table

Breakup of Shearless Meanders and "Outer" Tori in the Standard Nontwist Map

The breakup of shearless invariant tori with winding number $\omega=[0,1,11,1,1,...]$ (in continued fraction representation) of the standard nontwist map is studied numerically using Greene's residue criterion. Tori of this winding number can assume the shape of meanders (folded-over invariant tori which are not graphs over the x-axis in $(x,y)$ phase space), whose breakup is the first point of focus here. Secondly, multiple shearless orbits of this winding number can exist, leading to a new type of breakup scenario. Results are discussed within the framework of the renormalization group for area-preserving maps. Regularity of the critical tori is also investigated.Comment: submitted to Chao

A shotgun approach to identifying immune evading excipients for biologics drugs

Not applicabl

Renormalization and destruction of 1/γ21/\gamma^2 tori in the standard nontwist map

Extending the work of del-Castillo-Negrete, Greene, and Morrison, Physica D {\bf 91}, 1 (1996) and {\bf 100}, 311 (1997) on the standard nontwist map, the breakup of an invariant torus with winding number equal to the inverse golden mean squared is studied. Improved numerical techniques provide the greater accuracy that is needed for this case. The new results are interpreted within the renormalization group framework by constructing a renormalization operator on the space of commuting map pairs, and by studying the fixed points of the so constructed operator.Comment: To be Submitted to Chao

Adamtsl2 deletion results in bronchial fibrillin microfibril accumulation and bronchial epithelial dysplasia: A novel mouse model providing insights on geleophysic dysplasia

Mutations in the secreted glycoprotein ADAMTSL2 cause recessive geleophysic dysplasia (GD) in humans and Musladin–Lueke syndrome (MLS) in dogs. GD is a severe, often lethal, condition presenting with short stature, brachydactyly, stiff skin, joint contractures, tracheal-bronchial stenosis and cardiac valve anomalies, whereas MLS is non-lethal and characterized by short stature and severe skin fibrosis. Although most mutations in fibrillin-1 (FBN1) cause Marfan syndrome (MFS), a microfibril disorder leading to transforming growth factor-β (TGFβ) dysregulation, domain-specific FBN1 mutations result in dominant GD. ADAMTSL2 has been previously shown to bind FBN1 and latent TGFβ-binding protein-1 (LTBP1). Here, we investigated mice with targeted Adamtsl2 inactivation as a new model for GD (Adamtsl2−/− mice). An intragenic lacZ reporter in these mice showed that ADAMTSL2 was produced exclusively by bronchial smooth muscle cells during embryonic lung development. Adamtsl2−/− mice, which died at birth, had severe bronchial epithelial dysplasia with abnormal glycogen-rich inclusions in bronchial epithelium resembling the cellular anomalies described previously in GD. An increase in microfibrils in the bronchial wall was associated with increased FBN2 and microfibril-associated glycoprotein-1 (MAGP1) staining, whereas LTBP1 staining was increased in bronchial epithelium. ADAMTSL2 was shown to bind directly to FBN2 with an affinity comparable to FBN1. The observed extracellular matrix (ECM) alterations were associated with increased bronchial epithelial TGFβ signaling at 17.5 days of gestation; however, treatment with TGFβ-neutralizing antibody did not correct the epithelial dysplasia. These investigations reveal a new function of ADAMTSL2 in modulating microfibril formation, and a previously unsuspected association with FBN2. Our studies suggest that the bronchial epithelial dysplasia accompanying microfibril dysregulation in Adamtsl2−/− mice cannot be reversed by TGFβ neutralization, and thus might be mediated by other mechanisms

Plug-and-play excipients: an opportunity waiting to be exploited

Not applicabl